Skip to main content
Erschienen in: Cancer and Metastasis Reviews 2-3/2014

01.09.2014

Recent progress on nutraceutical research in prostate cancer

verfasst von: Yiwei Li, Aamir Ahmad, Dejuan Kong, Bin Bao, Fazlul H. Sarkar

Erschienen in: Cancer and Metastasis Reviews | Ausgabe 2-3/2014

Einloggen, um Zugang zu erhalten

Abstract

Recently, nutraceuticals have received increasing attention as the agents for cancer prevention and supplement with conventional therapy. Prostate cancer (PCa) is the most frequently diagnosed cancer and second leading cause of cancer-related death in men in the US. Growing evidences from epidemiological studies, in vitro experimental studies, animal studies, and clinical trials have shown that nutraceuticals could be very useful for the prevention and treatment of PCa. Several nutraceuticals including isoflavone, indole-3-carbinol, 3,3′-diindolylmethane, lycopene, (−)-epigallocatechin-3-gallate, and curcumin are known to downregulate the signal transductions in AR, Akt, NF-κB, and other signal transduction pathways which are vital for the development of PCa and the progression of PCa from androgen-sensitive to castrate-resistant PCa. Therefore, nutraceutical treatment in combination with conventional therapeutics could achieve better treatment outcome in prostate cancer therapy. Interestingly, some nutraceuticals could regulate the function of cancer stem cell (CSC)-related miRNAs and associated molecules, leading to the inhibition of prostatic CSCs which are responsible for drug resistance, tumor progression, and recurrence of PCa. Hence, nutraceuticals may serve as powerful agents for the prevention of PCa progression and they could also be useful in combination with chemotherapeutics or radiotherapy. Such strategy could become a promising newer approach for the treatment of metastatic PCa with better treatment outcome by improving overall survival.
Literatur
1.
Zurück zum Zitat Siegel, R., Naishadham, D., & Jemal, A. (2013). Cancer statistics, 2013. CA Cancer J Clin, 63, 11–30.PubMedCrossRef Siegel, R., Naishadham, D., & Jemal, A. (2013). Cancer statistics, 2013. CA Cancer J Clin, 63, 11–30.PubMedCrossRef
2.
Zurück zum Zitat Kolonel, L. N., Hankin, J. H., Whittemore, A. S., et al. (2000). Vegetables, fruits, legumes and prostate cancer: a multiethnic case–control study. Cancer Epidemiol Biomarkers Prev, 9, 795–804.PubMed Kolonel, L. N., Hankin, J. H., Whittemore, A. S., et al. (2000). Vegetables, fruits, legumes and prostate cancer: a multiethnic case–control study. Cancer Epidemiol Biomarkers Prev, 9, 795–804.PubMed
3.
Zurück zum Zitat Namiki, M., Akaza, H., Lee, S. E., et al. (2010). Prostate cancer working group report. Jpn J Clin Oncol, 40(Suppl 1), i70–i75.PubMedCrossRef Namiki, M., Akaza, H., Lee, S. E., et al. (2010). Prostate cancer working group report. Jpn J Clin Oncol, 40(Suppl 1), i70–i75.PubMedCrossRef
4.
Zurück zum Zitat Brower, V. (1998). Nutraceuticals: poised for a healthy slice of the healthcare market? Nat Biotechnol, 16, 728–731.PubMedCrossRef Brower, V. (1998). Nutraceuticals: poised for a healthy slice of the healthcare market? Nat Biotechnol, 16, 728–731.PubMedCrossRef
5.
Zurück zum Zitat Yan, L., & Spitznagel, E. L. (2009). Soy consumption and prostate cancer risk in men: a revisit of a meta-analysis. Am J Clin Nutr, 89, 1155–1163.PubMedCrossRef Yan, L., & Spitznagel, E. L. (2009). Soy consumption and prostate cancer risk in men: a revisit of a meta-analysis. Am J Clin Nutr, 89, 1155–1163.PubMedCrossRef
6.
Zurück zum Zitat Jacobsen, B. K., Knutsen, S. F., & Fraser, G. E. (1998). Does high soy milk intake reduce prostate cancer incidence? The Adventist Health Study (United States). Cancer Causes Control, 9, 553–557.PubMedCrossRef Jacobsen, B. K., Knutsen, S. F., & Fraser, G. E. (1998). Does high soy milk intake reduce prostate cancer incidence? The Adventist Health Study (United States). Cancer Causes Control, 9, 553–557.PubMedCrossRef
7.
Zurück zum Zitat Kurahashi, N., Iwasaki, M., Sasazuki, S., et al. (2007). Soy product and isoflavone consumption in relation to prostate cancer in Japanese men. Cancer Epidemiol Biomarkers Prev, 16, 538–545.PubMedCrossRef Kurahashi, N., Iwasaki, M., Sasazuki, S., et al. (2007). Soy product and isoflavone consumption in relation to prostate cancer in Japanese men. Cancer Epidemiol Biomarkers Prev, 16, 538–545.PubMedCrossRef
8.
Zurück zum Zitat Lee, M. M., Gomez, S. L., Chang, J. S., et al. (2003). Soy and isoflavone consumption in relation to prostate cancer risk in China. Cancer Epidemiol Biomarkers Prev, 12, 665–668.PubMed Lee, M. M., Gomez, S. L., Chang, J. S., et al. (2003). Soy and isoflavone consumption in relation to prostate cancer risk in China. Cancer Epidemiol Biomarkers Prev, 12, 665–668.PubMed
9.
Zurück zum Zitat Liu, B., Mao, Q., Cao, M., et al. (2012). Cruciferous vegetables intake and risk of prostate cancer: a meta-analysis. Int J Urol, 19, 134–141.PubMedCrossRef Liu, B., Mao, Q., Cao, M., et al. (2012). Cruciferous vegetables intake and risk of prostate cancer: a meta-analysis. Int J Urol, 19, 134–141.PubMedCrossRef
10.
Zurück zum Zitat Cohen, J. H., Kristal, A. R., & Stanford, J. L. (2000). Fruit and vegetable intakes and prostate cancer risk. J Natl Cancer Inst, 92, 61–68.PubMedCrossRef Cohen, J. H., Kristal, A. R., & Stanford, J. L. (2000). Fruit and vegetable intakes and prostate cancer risk. J Natl Cancer Inst, 92, 61–68.PubMedCrossRef
11.
Zurück zum Zitat Richman, E. L., Carroll, P. R., & Chan, J. M. (2012). Vegetable and fruit intake after diagnosis and risk of prostate cancer progression. Int J Cancer, 131, 201–210.PubMedCentralPubMedCrossRef Richman, E. L., Carroll, P. R., & Chan, J. M. (2012). Vegetable and fruit intake after diagnosis and risk of prostate cancer progression. Int J Cancer, 131, 201–210.PubMedCentralPubMedCrossRef
12.
Zurück zum Zitat Kirsh, V. A., Peters, U., Mayne, S. T., et al. (2007). Prospective study of fruit and vegetable intake and risk of prostate cancer. J Natl Cancer Inst, 99, 1200–1209.PubMedCrossRef Kirsh, V. A., Peters, U., Mayne, S. T., et al. (2007). Prospective study of fruit and vegetable intake and risk of prostate cancer. J Natl Cancer Inst, 99, 1200–1209.PubMedCrossRef
13.
Zurück zum Zitat Gann, P. H., Ma, J., Giovannucci, E., et al. (1999). Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis. Cancer Res, 59, 1225–1230.PubMed Gann, P. H., Ma, J., Giovannucci, E., et al. (1999). Lower prostate cancer risk in men with elevated plasma lycopene levels: results of a prospective analysis. Cancer Res, 59, 1225–1230.PubMed
14.
Zurück zum Zitat Lu, Q. Y., Hung, J. C., Heber, D., et al. (2001). Inverse associations between plasma lycopene and other carotenoids and prostate cancer. Cancer Epidemiol Biomarkers Prev, 10, 749–756.PubMed Lu, Q. Y., Hung, J. C., Heber, D., et al. (2001). Inverse associations between plasma lycopene and other carotenoids and prostate cancer. Cancer Epidemiol Biomarkers Prev, 10, 749–756.PubMed
15.
Zurück zum Zitat Giovannucci, E., Rimm, E. B., Liu, Y., et al. (2002). A prospective study of tomato products, lycopene, and prostate cancer risk. J Natl Cancer Inst, 94, 391–398.PubMedCrossRef Giovannucci, E., Rimm, E. B., Liu, Y., et al. (2002). A prospective study of tomato products, lycopene, and prostate cancer risk. J Natl Cancer Inst, 94, 391–398.PubMedCrossRef
16.
Zurück zum Zitat Etminan, M., Takkouche, B., & Caamano-Isorna, F. (2004). The role of tomato products and lycopene in the prevention of prostate cancer: a meta-analysis of observational studies. Cancer Epidemiol Biomarkers Prev, 13, 340–345.PubMed Etminan, M., Takkouche, B., & Caamano-Isorna, F. (2004). The role of tomato products and lycopene in the prevention of prostate cancer: a meta-analysis of observational studies. Cancer Epidemiol Biomarkers Prev, 13, 340–345.PubMed
17.
Zurück zum Zitat Peters, U., Leitzmann, M. F., Chatterjee, N., et al. (2007). Serum lycopene, other carotenoids, and prostate cancer risk: a nested case–control study in the prostate, lung, colorectal, and ovarian cancer screening trial. Cancer Epidemiol Biomarkers Prev, 16, 962–968.PubMedCrossRef Peters, U., Leitzmann, M. F., Chatterjee, N., et al. (2007). Serum lycopene, other carotenoids, and prostate cancer risk: a nested case–control study in the prostate, lung, colorectal, and ovarian cancer screening trial. Cancer Epidemiol Biomarkers Prev, 16, 962–968.PubMedCrossRef
18.
Zurück zum Zitat Mazdak, H., Mazdak, M., Jamali, L., et al. (2012). Determination of prostate cancer risk factors in Isfahan, Iran: a case–control study. Med Arh, 66, 45–48.PubMedCrossRef Mazdak, H., Mazdak, M., Jamali, L., et al. (2012). Determination of prostate cancer risk factors in Isfahan, Iran: a case–control study. Med Arh, 66, 45–48.PubMedCrossRef
19.
Zurück zum Zitat Salem, S., Salahi, M., Mohseni, M., et al. (2011). Major dietary factors and prostate cancer risk: a prospective multicenter case–control study. Nutr Cancer, 63, 21–27.PubMed Salem, S., Salahi, M., Mohseni, M., et al. (2011). Major dietary factors and prostate cancer risk: a prospective multicenter case–control study. Nutr Cancer, 63, 21–27.PubMed
20.
Zurück zum Zitat Jian, L., Xie, L. P., Lee, A. H., et al. (2004). Protective effect of green tea against prostate cancer: a case–control study in southeast China. Int J Cancer, 108, 130–135.PubMedCrossRef Jian, L., Xie, L. P., Lee, A. H., et al. (2004). Protective effect of green tea against prostate cancer: a case–control study in southeast China. Int J Cancer, 108, 130–135.PubMedCrossRef
21.
Zurück zum Zitat Kurahashi, N., Sasazuki, S., Iwasaki, M., et al. (2008). Green tea consumption and prostate cancer risk in Japanese men: a prospective study. Am J Epidemiol, 167, 71–77.PubMedCrossRef Kurahashi, N., Sasazuki, S., Iwasaki, M., et al. (2008). Green tea consumption and prostate cancer risk in Japanese men: a prospective study. Am J Epidemiol, 167, 71–77.PubMedCrossRef
22.
Zurück zum Zitat Kikuchi, N., Ohmori, K., Shimazu, T., et al. (2006). No association between green tea and prostate cancer risk in Japanese men: the Ohsaki Cohort Study. Br J Cancer, 95, 371–373.PubMedCentralPubMedCrossRef Kikuchi, N., Ohmori, K., Shimazu, T., et al. (2006). No association between green tea and prostate cancer risk in Japanese men: the Ohsaki Cohort Study. Br J Cancer, 95, 371–373.PubMedCentralPubMedCrossRef
23.
Zurück zum Zitat Zheng, J., Yang, B., Huang, T., et al. (2011). Green tea and black tea consumption and prostate cancer risk: an exploratory meta-analysis of observational studies. Nutr Cancer, 63, 663–672.PubMedCrossRef Zheng, J., Yang, B., Huang, T., et al. (2011). Green tea and black tea consumption and prostate cancer risk: an exploratory meta-analysis of observational studies. Nutr Cancer, 63, 663–672.PubMedCrossRef
24.
Zurück zum Zitat Jian, L., Lee, A. H., & Binns, C. W. (2007). Tea and lycopene protect against prostate cancer. Asia Pac J Clin Nutr, 16(Suppl 1), 453–457.PubMed Jian, L., Lee, A. H., & Binns, C. W. (2007). Tea and lycopene protect against prostate cancer. Asia Pac J Clin Nutr, 16(Suppl 1), 453–457.PubMed
25.
Zurück zum Zitat Jain, R. V., Mills, P. K., & Parikh-Patel, A. (2005). Cancer incidence in the south Asian population of California, 1988–2000. J Carcinog, 4, 21.PubMedCentralPubMedCrossRef Jain, R. V., Mills, P. K., & Parikh-Patel, A. (2005). Cancer incidence in the south Asian population of California, 1988–2000. J Carcinog, 4, 21.PubMedCentralPubMedCrossRef
26.
Zurück zum Zitat Donovan, M. J., Osman, I., Khan, F. M., et al. (2010). Androgen receptor expression is associated with prostate cancer-specific survival in castrate patients with metastatic disease. BJU Int, 105, 462–467.PubMedCrossRef Donovan, M. J., Osman, I., Khan, F. M., et al. (2010). Androgen receptor expression is associated with prostate cancer-specific survival in castrate patients with metastatic disease. BJU Int, 105, 462–467.PubMedCrossRef
27.
Zurück zum Zitat Sircar, K., Yoshimoto, M., Monzon, F. A., et al. (2009). PTEN genomic deletion is associated with p-Akt and AR signaling in poorer outcome, hormone refractory prostate cancer. J Pathol, 218, 505–513.PubMedCrossRef Sircar, K., Yoshimoto, M., Monzon, F. A., et al. (2009). PTEN genomic deletion is associated with p-Akt and AR signaling in poorer outcome, hormone refractory prostate cancer. J Pathol, 218, 505–513.PubMedCrossRef
28.
Zurück zum Zitat Attar, R. M., Takimoto, C. H., & Gottardis, M. M. (2009). Castration-resistant prostate cancer: locking up the molecular escape routes. Clin Cancer Res, 15, 3251–3255.PubMedCrossRef Attar, R. M., Takimoto, C. H., & Gottardis, M. M. (2009). Castration-resistant prostate cancer: locking up the molecular escape routes. Clin Cancer Res, 15, 3251–3255.PubMedCrossRef
29.
Zurück zum Zitat Debes, J. D., & Tindall, D. J. (2004). Mechanisms of androgen-refractory prostate cancer. N Engl J Med, 351, 1488–1490.PubMedCrossRef Debes, J. D., & Tindall, D. J. (2004). Mechanisms of androgen-refractory prostate cancer. N Engl J Med, 351, 1488–1490.PubMedCrossRef
30.
Zurück zum Zitat Oh, H. Y., Leem, J., Yoon, S. J., et al. (2010). Lipid raft cholesterol and genistein inhibit the cell viability of prostate cancer cells via the partial contribution of EGFR-Akt/p70S6k pathway and downregulation of androgen receptor. Biochem Biophys Res Commun, 393, 319–324.PubMedCrossRef Oh, H. Y., Leem, J., Yoon, S. J., et al. (2010). Lipid raft cholesterol and genistein inhibit the cell viability of prostate cancer cells via the partial contribution of EGFR-Akt/p70S6k pathway and downregulation of androgen receptor. Biochem Biophys Res Commun, 393, 319–324.PubMedCrossRef
31.
Zurück zum Zitat Basak, S., Pookot, D., Noonan, E. J., et al. (2008). Genistein downregulates androgen receptor by modulating HDAC6-Hsp90 chaperone function. Mol Cancer Ther, 7, 3195–3202.PubMedCrossRef Basak, S., Pookot, D., Noonan, E. J., et al. (2008). Genistein downregulates androgen receptor by modulating HDAC6-Hsp90 chaperone function. Mol Cancer Ther, 7, 3195–3202.PubMedCrossRef
32.
Zurück zum Zitat Li, Y., Wang, Z., Kong, D., et al. (2008). Regulation of Akt/FOXO3a/GSK-3beta/AR signaling network by isoflavone in prostate cancer cells. J Biol Chem, 283, 27707–27716.PubMedCentralPubMedCrossRef Li, Y., Wang, Z., Kong, D., et al. (2008). Regulation of Akt/FOXO3a/GSK-3beta/AR signaling network by isoflavone in prostate cancer cells. J Biol Chem, 283, 27707–27716.PubMedCentralPubMedCrossRef
33.
Zurück zum Zitat Jagadeesh, S., Kyo, S., & Banerjee, P. P. (2006). Genistein represses telomerase activity via both transcriptional and posttranslational mechanisms in human prostate cancer cells. Cancer Res, 66, 2107–2115.PubMedCrossRef Jagadeesh, S., Kyo, S., & Banerjee, P. P. (2006). Genistein represses telomerase activity via both transcriptional and posttranslational mechanisms in human prostate cancer cells. Cancer Res, 66, 2107–2115.PubMedCrossRef
34.
Zurück zum Zitat Li, Y., Ahmed, F., Ali, S., et al. (2005). Inactivation of nuclear factor kappaB by soy isoflavone genistein contributes to increased apoptosis induced by chemotherapeutic agents in human cancer cells. Cancer Res, 65, 6934–6942.PubMedCrossRef Li, Y., Ahmed, F., Ali, S., et al. (2005). Inactivation of nuclear factor kappaB by soy isoflavone genistein contributes to increased apoptosis induced by chemotherapeutic agents in human cancer cells. Cancer Res, 65, 6934–6942.PubMedCrossRef
35.
Zurück zum Zitat Wang, Y., Wang, H., Zhang, W., et al. (2013). Genistein sensitizes bladder cancer cells to HCPT treatment in vitro and in vivo via ATM/NF-kappaB/IKK pathway-induced apoptosis. PLoS One, 8, e50175.PubMedCentralPubMedCrossRef Wang, Y., Wang, H., Zhang, W., et al. (2013). Genistein sensitizes bladder cancer cells to HCPT treatment in vitro and in vivo via ATM/NF-kappaB/IKK pathway-induced apoptosis. PLoS One, 8, e50175.PubMedCentralPubMedCrossRef
36.
Zurück zum Zitat Legg, R. L., Tolman, J. R., Lovinger, C. T., et al. (2008). Diets high in selenium and isoflavones decrease androgen-regulated gene expression in healthy rat dorsolateral prostate. Reprod Biol Endocrinol, 6, 57.PubMedCentralPubMedCrossRef Legg, R. L., Tolman, J. R., Lovinger, C. T., et al. (2008). Diets high in selenium and isoflavones decrease androgen-regulated gene expression in healthy rat dorsolateral prostate. Reprod Biol Endocrinol, 6, 57.PubMedCentralPubMedCrossRef
37.
Zurück zum Zitat Fritz, W. A., Wang, J., Eltoum, I. E., et al. (2002). Dietary genistein downregulates androgen and estrogen receptor expression in the rat prostate. Mol Cell Endocrinol, 186, 89–99.PubMedCrossRef Fritz, W. A., Wang, J., Eltoum, I. E., et al. (2002). Dietary genistein downregulates androgen and estrogen receptor expression in the rat prostate. Mol Cell Endocrinol, 186, 89–99.PubMedCrossRef
38.
Zurück zum Zitat Phillip, C. J., Giardina, C. K., Bilir, B., et al. (2012). Genistein cooperates with the histone deacetylase inhibitor vorinostat to induce cell death in prostate cancer cells. BMC Cancer, 12, 145.PubMedCentralPubMedCrossRef Phillip, C. J., Giardina, C. K., Bilir, B., et al. (2012). Genistein cooperates with the histone deacetylase inhibitor vorinostat to induce cell death in prostate cancer cells. BMC Cancer, 12, 145.PubMedCentralPubMedCrossRef
39.
Zurück zum Zitat Zhang, L., Li, L., Jiao, M., et al. (2012). Genistein inhibits the stemness properties of prostate cancer cells through targeting Hedgehog-Gli1 pathway. Cancer Lett, 323, 48–57.PubMedCrossRef Zhang, L., Li, L., Jiao, M., et al. (2012). Genistein inhibits the stemness properties of prostate cancer cells through targeting Hedgehog-Gli1 pathway. Cancer Lett, 323, 48–57.PubMedCrossRef
40.
Zurück zum Zitat Chang, K. L., Cheng, H. L., Huang, L. W., et al. (2009). Combined effects of terazosin and genistein on a metastatic, hormone-independent human prostate cancer cell line. Cancer Lett, 276, 14–20.PubMedCrossRef Chang, K. L., Cheng, H. L., Huang, L. W., et al. (2009). Combined effects of terazosin and genistein on a metastatic, hormone-independent human prostate cancer cell line. Cancer Lett, 276, 14–20.PubMedCrossRef
41.
Zurück zum Zitat Burich, R. A., Holland, W. S., Vinall, R. L., et al. (2008). Genistein combined polysaccharide enhances activity of docetaxel, bicalutamide, and Src kinase inhibition in androgen-dependent and independent prostate cancer cell lines. BJU Int, 102, 1458–1466.PubMed Burich, R. A., Holland, W. S., Vinall, R. L., et al. (2008). Genistein combined polysaccharide enhances activity of docetaxel, bicalutamide, and Src kinase inhibition in androgen-dependent and independent prostate cancer cell lines. BJU Int, 102, 1458–1466.PubMed
42.
Zurück zum Zitat Wang, Y., Raffoul, J. J., Che, M., et al. (2006). Prostate cancer treatment is enhanced by genistein in vitro and in vivo in a syngeneic orthotopic tumor model. Radiat Res, 166, 73–80.PubMedCrossRef Wang, Y., Raffoul, J. J., Che, M., et al. (2006). Prostate cancer treatment is enhanced by genistein in vitro and in vivo in a syngeneic orthotopic tumor model. Radiat Res, 166, 73–80.PubMedCrossRef
43.
Zurück zum Zitat Raffoul, J. J., Wang, Y., Kucuk, O., et al. (2006). Genistein inhibits radiation-induced activation of NF-kappaB in prostate cancer cells promoting apoptosis and G2/M cell cycle arrest. BMC Cancer, 6, 107.PubMedCentralPubMedCrossRef Raffoul, J. J., Wang, Y., Kucuk, O., et al. (2006). Genistein inhibits radiation-induced activation of NF-kappaB in prostate cancer cells promoting apoptosis and G2/M cell cycle arrest. BMC Cancer, 6, 107.PubMedCentralPubMedCrossRef
44.
Zurück zum Zitat Singh-Gupta, V., Zhang, H., Banerjee, S., et al. (2009). Radiation-induced HIF-1alpha cell survival pathway is inhibited by soy isoflavones in prostate cancer cells. Int J Cancer, 124, 1675–1684.PubMedCentralPubMedCrossRef Singh-Gupta, V., Zhang, H., Banerjee, S., et al. (2009). Radiation-induced HIF-1alpha cell survival pathway is inhibited by soy isoflavones in prostate cancer cells. Int J Cancer, 124, 1675–1684.PubMedCentralPubMedCrossRef
45.
Zurück zum Zitat Busby, M. G., Jeffcoat, A. R., Bloedon, L. T., et al. (2002). Clinical characteristics and pharmacokinetics of purified soy isoflavones: single-dose administration to healthy men. Am J Clin Nutr, 75, 126–136.PubMed Busby, M. G., Jeffcoat, A. R., Bloedon, L. T., et al. (2002). Clinical characteristics and pharmacokinetics of purified soy isoflavones: single-dose administration to healthy men. Am J Clin Nutr, 75, 126–136.PubMed
46.
Zurück zum Zitat Fischer, L., Mahoney, C., Jeffcoat, A. R., et al. (2004). Clinical characteristics and pharmacokinetics of purified soy isoflavones: multiple-dose administration to men with prostate neoplasia. Nutr Cancer, 48, 160–170.PubMedCrossRef Fischer, L., Mahoney, C., Jeffcoat, A. R., et al. (2004). Clinical characteristics and pharmacokinetics of purified soy isoflavones: multiple-dose administration to men with prostate neoplasia. Nutr Cancer, 48, 160–170.PubMedCrossRef
47.
Zurück zum Zitat Kumar, N. B., Cantor, A., Allen, K., et al. (2004). The specific role of isoflavones in reducing prostate cancer risk. Prostate, 59, 141–147.PubMedCrossRef Kumar, N. B., Cantor, A., Allen, K., et al. (2004). The specific role of isoflavones in reducing prostate cancer risk. Prostate, 59, 141–147.PubMedCrossRef
48.
Zurück zum Zitat Kumar, N. B., Krischer, J. P., Allen, K., et al. (2007). Safety of purified isoflavones in men with clinically localized prostate cancer. Nutr Cancer, 59, 169–175.PubMedCentralPubMedCrossRef Kumar, N. B., Krischer, J. P., Allen, K., et al. (2007). Safety of purified isoflavones in men with clinically localized prostate cancer. Nutr Cancer, 59, 169–175.PubMedCentralPubMedCrossRef
49.
Zurück zum Zitat Kumar, N. B., Krischer, J. P., Allen, K., et al. (2007). A phase II randomized, placebo-controlled clinical trial of purified isoflavones in modulating steroid hormones in men diagnosed with localized prostate cancer. Nutr Cancer, 59, 163–168.PubMedCentralPubMedCrossRef Kumar, N. B., Krischer, J. P., Allen, K., et al. (2007). A phase II randomized, placebo-controlled clinical trial of purified isoflavones in modulating steroid hormones in men diagnosed with localized prostate cancer. Nutr Cancer, 59, 163–168.PubMedCentralPubMedCrossRef
50.
Zurück zum Zitat Takimoto, C. H., Glover, K., Huang, X., et al. (2003). Phase I pharmacokinetic and pharmacodynamic analysis of unconjugated soy isoflavones administered to individuals with cancer. Cancer Epidemiol Biomarkers Prev, 12, 1213–1221.PubMed Takimoto, C. H., Glover, K., Huang, X., et al. (2003). Phase I pharmacokinetic and pharmacodynamic analysis of unconjugated soy isoflavones administered to individuals with cancer. Cancer Epidemiol Biomarkers Prev, 12, 1213–1221.PubMed
51.
Zurück zum Zitat Hussain, M., Banerjee, M., Sarkar, F. H., et al. (2003). Soy isoflavones in the treatment of prostate cancer. Nutr Cancer, 47, 111–117.PubMedCrossRef Hussain, M., Banerjee, M., Sarkar, F. H., et al. (2003). Soy isoflavones in the treatment of prostate cancer. Nutr Cancer, 47, 111–117.PubMedCrossRef
52.
Zurück zum Zitat Bhuiyan, M. M., Li, Y., Banerjee, S., et al. (2006). Downregulation of androgen receptor by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells. Cancer Res, 66, 10064–10072.PubMedCrossRef Bhuiyan, M. M., Li, Y., Banerjee, S., et al. (2006). Downregulation of androgen receptor by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in both hormone-sensitive LNCaP and insensitive C4-2B prostate cancer cells. Cancer Res, 66, 10064–10072.PubMedCrossRef
53.
Zurück zum Zitat Hsu, J. C., Zhang, J., Dev, A., et al. (2005). Indole-3-carbinol inhibition of androgen receptor expression and downregulation of androgen responsiveness in human prostate cancer cells. Carcinogenesis, 26, 1896–1904.PubMedCrossRef Hsu, J. C., Zhang, J., Dev, A., et al. (2005). Indole-3-carbinol inhibition of androgen receptor expression and downregulation of androgen responsiveness in human prostate cancer cells. Carcinogenesis, 26, 1896–1904.PubMedCrossRef
54.
Zurück zum Zitat Le, H. T., Schaldach, C. M., Firestone, G. L., et al. (2003). Plant-derived 3,3′-diindolylmethane is a strong androgen antagonist in human prostate cancer cells. J Biol Chem, 278, 21136–21145.PubMedCrossRef Le, H. T., Schaldach, C. M., Firestone, G. L., et al. (2003). Plant-derived 3,3′-diindolylmethane is a strong androgen antagonist in human prostate cancer cells. J Biol Chem, 278, 21136–21145.PubMedCrossRef
55.
Zurück zum Zitat Li, Y., Wang, Z., Kong, D., et al. (2007). Regulation of FOXO3a/beta-catenin/GSK-3beta signaling by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in prostate cancer cells. J Biol Chem, 282, 21542–21550.PubMedCrossRef Li, Y., Wang, Z., Kong, D., et al. (2007). Regulation of FOXO3a/beta-catenin/GSK-3beta signaling by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in prostate cancer cells. J Biol Chem, 282, 21542–21550.PubMedCrossRef
56.
Zurück zum Zitat Li, Y., Kong, D., Wang, Z., et al. (2011). Inactivation of AR/TMPRSS2-ERG/Wnt signaling networks attenuates the aggressive behavior of prostate cancer cells. Cancer Prev Res (Phila), 4, 1495–1506.CrossRef Li, Y., Kong, D., Wang, Z., et al. (2011). Inactivation of AR/TMPRSS2-ERG/Wnt signaling networks attenuates the aggressive behavior of prostate cancer cells. Cancer Prev Res (Phila), 4, 1495–1506.CrossRef
57.
Zurück zum Zitat Li, Y., Chinni, S. R., & Sarkar, F. H. (2005). Selective growth regulatory and proapoptotic effects of DIM is mediated by AKT and NF-kappaB pathways in prostate cancer cells. Front Biosci, 10, 236–243.PubMedCrossRef Li, Y., Chinni, S. R., & Sarkar, F. H. (2005). Selective growth regulatory and proapoptotic effects of DIM is mediated by AKT and NF-kappaB pathways in prostate cancer cells. Front Biosci, 10, 236–243.PubMedCrossRef
58.
Zurück zum Zitat Wang, T. T., Schoene, N. W., Milner, J. A., et al. (2012). Broccoli-derived phytochemicals indole-3-carbinol and 3,3′-diindolylmethane exerts concentration-dependent pleiotropic effects on prostate cancer cells: comparison with other cancer-preventive phytochemicals. Mol Carcinog, 51, 244–256.PubMedCrossRef Wang, T. T., Schoene, N. W., Milner, J. A., et al. (2012). Broccoli-derived phytochemicals indole-3-carbinol and 3,3′-diindolylmethane exerts concentration-dependent pleiotropic effects on prostate cancer cells: comparison with other cancer-preventive phytochemicals. Mol Carcinog, 51, 244–256.PubMedCrossRef
59.
Zurück zum Zitat Ahmad, A., Kong, D., Sarkar, S. H., et al. (2009). Inactivation of uPA and its receptor uPAR by 3,3′-diindolylmethane (DIM) leads to the inhibition of prostate cancer cell growth and migration. J Cell Biochem, 107, 516–527.PubMedCentralPubMedCrossRef Ahmad, A., Kong, D., Sarkar, S. H., et al. (2009). Inactivation of uPA and its receptor uPAR by 3,3′-diindolylmethane (DIM) leads to the inhibition of prostate cancer cell growth and migration. J Cell Biochem, 107, 516–527.PubMedCentralPubMedCrossRef
60.
Zurück zum Zitat Azmi, A. S., Ahmad, A., Banerjee, S., et al. (2008). Chemoprevention of pancreatic cancer: characterization of Par-4 and its modulation by 3,3′ diindolylmethane (DIM). Pharm Res, 25, 2117–2124.PubMedCentralPubMedCrossRef Azmi, A. S., Ahmad, A., Banerjee, S., et al. (2008). Chemoprevention of pancreatic cancer: characterization of Par-4 and its modulation by 3,3′ diindolylmethane (DIM). Pharm Res, 25, 2117–2124.PubMedCentralPubMedCrossRef
61.
Zurück zum Zitat Beaver, L. M., Yu, T. W., Sokolowski, E. I., et al. (2012). 3,3′-Diindolylmethane, but not indole-3-carbinol, inhibits histone deacetylase activity in prostate cancer cells. Toxicol Appl Pharmacol, 263, 345–351.PubMedCentralPubMedCrossRef Beaver, L. M., Yu, T. W., Sokolowski, E. I., et al. (2012). 3,3′-Diindolylmethane, but not indole-3-carbinol, inhibits histone deacetylase activity in prostate cancer cells. Toxicol Appl Pharmacol, 263, 345–351.PubMedCentralPubMedCrossRef
62.
Zurück zum Zitat Chen, D., Banerjee, S., Cui, Q. C., et al. (2012). Activation of AMP-activated protein kinase by 3,3′-diindolylmethane (DIM) is associated with human prostate cancer cell death in vitro and in vivo. PLoS One, 7, e47186.PubMedCentralPubMedCrossRef Chen, D., Banerjee, S., Cui, Q. C., et al. (2012). Activation of AMP-activated protein kinase by 3,3′-diindolylmethane (DIM) is associated with human prostate cancer cell death in vitro and in vivo. PLoS One, 7, e47186.PubMedCentralPubMedCrossRef
63.
Zurück zum Zitat Duhon, D., Bigelow, R. L., Coleman, D. T., et al. (2010). The polyphenol epigallocatechin-3-gallate affects lipid rafts to block activation of the c-Met receptor in prostate cancer cells. Mol Carcinog, 49, 739–749.PubMed Duhon, D., Bigelow, R. L., Coleman, D. T., et al. (2010). The polyphenol epigallocatechin-3-gallate affects lipid rafts to block activation of the c-Met receptor in prostate cancer cells. Mol Carcinog, 49, 739–749.PubMed
64.
Zurück zum Zitat Kong, D., Li, Y., Wang, Z., et al. (2007). Inhibition of angiogenesis and invasion by 3,3′-diindolylmethane is mediated by the nuclear factor-kappaB downstream target genes MMP-9 and uPA that regulated bioavailability of vascular endothelial growth factor in prostate cancer. Cancer Res, 67, 3310–3319.PubMedCrossRef Kong, D., Li, Y., Wang, Z., et al. (2007). Inhibition of angiogenesis and invasion by 3,3′-diindolylmethane is mediated by the nuclear factor-kappaB downstream target genes MMP-9 and uPA that regulated bioavailability of vascular endothelial growth factor in prostate cancer. Cancer Res, 67, 3310–3319.PubMedCrossRef
65.
Zurück zum Zitat Kong, D., Heath, E., Chen, W., et al. (2012). Loss of let-7 upregulates EZH2 in prostate cancer consistent with the acquisition of cancer stem cell signatures that are attenuated by BR-DIM. PLoS One, 7, e33729.PubMedCentralPubMedCrossRef Kong, D., Heath, E., Chen, W., et al. (2012). Loss of let-7 upregulates EZH2 in prostate cancer consistent with the acquisition of cancer stem cell signatures that are attenuated by BR-DIM. PLoS One, 7, e33729.PubMedCentralPubMedCrossRef
66.
Zurück zum Zitat Fan, S., Meng, Q., Auborn, K., et al. (2006). BRCA1 and BRCA2 as molecular targets for phytochemicals indole-3-carbinol and genistein in breast and prostate cancer cells. Br J Cancer, 94, 407–426.PubMedCentralPubMedCrossRef Fan, S., Meng, Q., Auborn, K., et al. (2006). BRCA1 and BRCA2 as molecular targets for phytochemicals indole-3-carbinol and genistein in breast and prostate cancer cells. Br J Cancer, 94, 407–426.PubMedCentralPubMedCrossRef
67.
Zurück zum Zitat Sarkar, F. H., & Li, Y. (2004). Indole-3-carbinol and prostate cancer. J Nutr, 134, 3493S–3498S.PubMed Sarkar, F. H., & Li, Y. (2004). Indole-3-carbinol and prostate cancer. J Nutr, 134, 3493S–3498S.PubMed
68.
Zurück zum Zitat Kumi-Diaka, J. (2002). Chemosensitivity of human prostate cancer cells PC3 and LNCaP to genistein isoflavone and beta-lapachone. Biol Cell, 94, 37–44.PubMedCrossRef Kumi-Diaka, J. (2002). Chemosensitivity of human prostate cancer cells PC3 and LNCaP to genistein isoflavone and beta-lapachone. Biol Cell, 94, 37–44.PubMedCrossRef
69.
Zurück zum Zitat Kumi-Diaka, J., Merchant, K., Haces, A., et al. (2010). Genistein-selenium combination induces growth arrest in prostate cancer cells. J Med Food, 13, 842–850.PubMedCrossRef Kumi-Diaka, J., Merchant, K., Haces, A., et al. (2010). Genistein-selenium combination induces growth arrest in prostate cancer cells. J Med Food, 13, 842–850.PubMedCrossRef
70.
Zurück zum Zitat Rahman, K. M., Banerjee, S., Ali, S., et al. (2009). 3,3′-Diindolylmethane enhances taxotere-induced apoptosis in hormone-refractory prostate cancer cells through survivin downregulation. Cancer Res, 69, 4468–4475.PubMedCrossRef Rahman, K. M., Banerjee, S., Ali, S., et al. (2009). 3,3′-Diindolylmethane enhances taxotere-induced apoptosis in hormone-refractory prostate cancer cells through survivin downregulation. Cancer Res, 69, 4468–4475.PubMedCrossRef
71.
Zurück zum Zitat Reed, G. A., Sunega, J. M., Sullivan, D. K., et al. (2008). Single-dose pharmacokinetics and tolerability of absorption-enhanced 3,3′-diindolylmethane in healthy subjects. Cancer Epidemiol Biomarkers Prev, 17, 2619–2624.PubMedCentralPubMedCrossRef Reed, G. A., Sunega, J. M., Sullivan, D. K., et al. (2008). Single-dose pharmacokinetics and tolerability of absorption-enhanced 3,3′-diindolylmethane in healthy subjects. Cancer Epidemiol Biomarkers Prev, 17, 2619–2624.PubMedCentralPubMedCrossRef
72.
Zurück zum Zitat Heath, E. I., Heilbrun, L. K., Li, J., et al. (2010). A phase I dose-escalation study of oral BR-DIM (BioResponse 3,3′-diindolylmethane) in castrate-resistant, non-metastatic prostate cancer. Am J Transl Res, 2, 402–411.PubMedCentralPubMed Heath, E. I., Heilbrun, L. K., Li, J., et al. (2010). A phase I dose-escalation study of oral BR-DIM (BioResponse 3,3′-diindolylmethane) in castrate-resistant, non-metastatic prostate cancer. Am J Transl Res, 2, 402–411.PubMedCentralPubMed
73.
Zurück zum Zitat Hadad, N., & Levy, R. (2012). The synergistic anti-inflammatory effects of lycopene, lutein, beta-carotene, and carnosic acid combinations via redox-based inhibition of NF-kappaB signaling. Free Radic Biol Med, 53, 1381–1391.PubMedCrossRef Hadad, N., & Levy, R. (2012). The synergistic anti-inflammatory effects of lycopene, lutein, beta-carotene, and carnosic acid combinations via redox-based inhibition of NF-kappaB signaling. Free Radic Biol Med, 53, 1381–1391.PubMedCrossRef
74.
Zurück zum Zitat Palozza, P., Colangelo, M., Simone, R., et al. (2010). Lycopene induces cell growth inhibition by altering mevalonate pathway and Ras signaling in cancer cell lines. Carcinogenesis, 31, 1813–1821.PubMedCrossRef Palozza, P., Colangelo, M., Simone, R., et al. (2010). Lycopene induces cell growth inhibition by altering mevalonate pathway and Ras signaling in cancer cell lines. Carcinogenesis, 31, 1813–1821.PubMedCrossRef
75.
Zurück zum Zitat Liu, X., Allen, J. D., Arnold, J. T., et al. (2008). Lycopene inhibits IGF-I signal transduction and growth in normal prostate epithelial cells by decreasing DHT-modulated IGF-I production in co-cultured reactive stromal cells. Carcinogenesis, 29, 816–823.PubMedCrossRef Liu, X., Allen, J. D., Arnold, J. T., et al. (2008). Lycopene inhibits IGF-I signal transduction and growth in normal prostate epithelial cells by decreasing DHT-modulated IGF-I production in co-cultured reactive stromal cells. Carcinogenesis, 29, 816–823.PubMedCrossRef
76.
Zurück zum Zitat Zhang, X., Wang, Q., Neil, B., et al. (2010). Effect of lycopene on androgen receptor and prostate-specific antigen velocity. Chin Med J (Engl), 123, 2231–2236. Zhang, X., Wang, Q., Neil, B., et al. (2010). Effect of lycopene on androgen receptor and prostate-specific antigen velocity. Chin Med J (Engl), 123, 2231–2236.
77.
Zurück zum Zitat Tang, Y., Parmakhtiar, B., Simoneau, A. R., et al. (2011). Lycopene enhances docetaxel's effect in castration-resistant prostate cancer associated with insulin-like growth factor I receptor levels. Neoplasia, 13, 108–119.PubMedCentralPubMed Tang, Y., Parmakhtiar, B., Simoneau, A. R., et al. (2011). Lycopene enhances docetaxel's effect in castration-resistant prostate cancer associated with insulin-like growth factor I receptor levels. Neoplasia, 13, 108–119.PubMedCentralPubMed
78.
Zurück zum Zitat Kumar, N. B., Besterman-Dahan, K., Kang, L., et al. (2008). Results of a randomized clinical trial of the action of several doses of lycopene in localized prostate cancer: administration prior to radical prostatectomy. Clin Med Urol, 1, 1–14.PubMedCentralPubMed Kumar, N. B., Besterman-Dahan, K., Kang, L., et al. (2008). Results of a randomized clinical trial of the action of several doses of lycopene in localized prostate cancer: administration prior to radical prostatectomy. Clin Med Urol, 1, 1–14.PubMedCentralPubMed
79.
Zurück zum Zitat Kucuk, O., Sarkar, F. H., Sakr, W., et al. (2001). Phase II randomized clinical trial of lycopene supplementation before radical prostatectomy. Cancer Epidemiol Biomarkers Prev, 10, 861–868.PubMed Kucuk, O., Sarkar, F. H., Sakr, W., et al. (2001). Phase II randomized clinical trial of lycopene supplementation before radical prostatectomy. Cancer Epidemiol Biomarkers Prev, 10, 861–868.PubMed
80.
Zurück zum Zitat Kucuk, O., Sarkar, F. H., Djuric, Z., et al. (2002). Effects of lycopene supplementation in patients with localized prostate cancer. Exp Biol Med (Maywood), 227, 881–885. Kucuk, O., Sarkar, F. H., Djuric, Z., et al. (2002). Effects of lycopene supplementation in patients with localized prostate cancer. Exp Biol Med (Maywood), 227, 881–885.
81.
Zurück zum Zitat Grainger, E. M., Schwartz, S. J., Wang, S., et al. (2008). A combination of tomato and soy products for men with recurring prostate cancer and rising prostate-specific antigen. Nutr Cancer, 60, 145–154.PubMedCrossRef Grainger, E. M., Schwartz, S. J., Wang, S., et al. (2008). A combination of tomato and soy products for men with recurring prostate cancer and rising prostate-specific antigen. Nutr Cancer, 60, 145–154.PubMedCrossRef
82.
Zurück zum Zitat Hastak, K., Gupta, S., Ahmad, N., et al. (2003). Role of p53 and NF-kappaB in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells. Oncogene, 22, 4851–4859.PubMedCrossRef Hastak, K., Gupta, S., Ahmad, N., et al. (2003). Role of p53 and NF-kappaB in epigallocatechin-3-gallate-induced apoptosis of LNCaP cells. Oncogene, 22, 4851–4859.PubMedCrossRef
83.
Zurück zum Zitat Vayalil, P. K., & Katiyar, S. K. (2004). Treatment of epigallocatechin-3-gallate inhibits matrix metalloproteinases-2 and -9 via inhibition of activation of mitogen-activated protein kinases, c-jun, and NF-kappaB in human prostate carcinoma DU-145 cells. Prostate, 59, 33–42.PubMedCrossRef Vayalil, P. K., & Katiyar, S. K. (2004). Treatment of epigallocatechin-3-gallate inhibits matrix metalloproteinases-2 and -9 via inhibition of activation of mitogen-activated protein kinases, c-jun, and NF-kappaB in human prostate carcinoma DU-145 cells. Prostate, 59, 33–42.PubMedCrossRef
84.
Zurück zum Zitat Siddiqui, I. A., Adhami, V. M., Afaq, F., et al. (2004). Modulation of phosphatidylinositol-3-kinase/protein kinase B- and mitogen-activated protein kinase-pathways by tea polyphenols in human prostate cancer cells. J Cell Biochem, 91, 232–242.PubMedCrossRef Siddiqui, I. A., Adhami, V. M., Afaq, F., et al. (2004). Modulation of phosphatidylinositol-3-kinase/protein kinase B- and mitogen-activated protein kinase-pathways by tea polyphenols in human prostate cancer cells. J Cell Biochem, 91, 232–242.PubMedCrossRef
85.
Zurück zum Zitat Ren, F., Zhang, S., Mitchell, S. H., et al. (2000). Tea polyphenols downregulate the expression of the androgen receptor in LNCaP prostate cancer cells. Oncogene, 19, 1924–1932.PubMedCrossRef Ren, F., Zhang, S., Mitchell, S. H., et al. (2000). Tea polyphenols downregulate the expression of the androgen receptor in LNCaP prostate cancer cells. Oncogene, 19, 1924–1932.PubMedCrossRef
86.
Zurück zum Zitat Siddiqui, I. A., Asim, M., Hafeez, B. B., et al. (2011). Green tea polyphenol EGCG blunts androgen receptor function in prostate cancer. FASEB J, 25, 1198–1207.PubMedCentralPubMedCrossRef Siddiqui, I. A., Asim, M., Hafeez, B. B., et al. (2011). Green tea polyphenol EGCG blunts androgen receptor function in prostate cancer. FASEB J, 25, 1198–1207.PubMedCentralPubMedCrossRef
87.
Zurück zum Zitat Lee, Y. H., Kwak, J., Choi, H. K., et al. (2012). EGCG suppresses prostate cancer cell growth modulating acetylation of androgen receptor by anti-histone acetyltransferase activity. Int J Mol Med, 30, 69–74.PubMed Lee, Y. H., Kwak, J., Choi, H. K., et al. (2012). EGCG suppresses prostate cancer cell growth modulating acetylation of androgen receptor by anti-histone acetyltransferase activity. Int J Mol Med, 30, 69–74.PubMed
88.
Zurück zum Zitat Stearns, M. E., Amatangelo, M. D., Varma, D., et al. (2010). Combination therapy with epigallocatechin-3-gallate and doxorubicin in human prostate tumor modeling studies: inhibition of metastatic tumor growth in severe combined immunodeficiency mice. Am J Pathol, 177, 3169–3179.PubMedCentralPubMedCrossRef Stearns, M. E., Amatangelo, M. D., Varma, D., et al. (2010). Combination therapy with epigallocatechin-3-gallate and doxorubicin in human prostate tumor modeling studies: inhibition of metastatic tumor growth in severe combined immunodeficiency mice. Am J Pathol, 177, 3169–3179.PubMedCentralPubMedCrossRef
89.
Zurück zum Zitat Stearns, M. E., & Wang, M. (2011). Synergistic effects of the green tea extract epigallocatechin-3-gallate and taxane in eradication of malignant human prostate tumors. Transl Oncol, 4, 147–156.PubMedCentralPubMedCrossRef Stearns, M. E., & Wang, M. (2011). Synergistic effects of the green tea extract epigallocatechin-3-gallate and taxane in eradication of malignant human prostate tumors. Transl Oncol, 4, 147–156.PubMedCentralPubMedCrossRef
90.
Zurück zum Zitat Siddiqui, I. A., Malik, A., Adhami, V. M., et al. (2008). Green tea polyphenol EGCG sensitizes human prostate carcinoma LNCaP cells to TRAIL-mediated apoptosis and synergistically inhibits biomarkers associated with angiogenesis and metastasis. Oncogene, 27, 2055–2063.PubMedCrossRef Siddiqui, I. A., Malik, A., Adhami, V. M., et al. (2008). Green tea polyphenol EGCG sensitizes human prostate carcinoma LNCaP cells to TRAIL-mediated apoptosis and synergistically inhibits biomarkers associated with angiogenesis and metastasis. Oncogene, 27, 2055–2063.PubMedCrossRef
91.
Zurück zum Zitat Adhami, V. M., Malik, A., Zaman, N., et al. (2007). Combined inhibitory effects of green tea polyphenols and selective cyclooxygenase-2 inhibitors on the growth of human prostate cancer cells both in vitro and in vivo. Clin Cancer Res, 13, 1611–1619.PubMedCrossRef Adhami, V. M., Malik, A., Zaman, N., et al. (2007). Combined inhibitory effects of green tea polyphenols and selective cyclooxygenase-2 inhibitors on the growth of human prostate cancer cells both in vitro and in vivo. Clin Cancer Res, 13, 1611–1619.PubMedCrossRef
92.
Zurück zum Zitat Wang, P., Aronson, W. J., Huang, M., et al. (2010). Green tea polyphenols and metabolites in prostatectomy tissue: implications for cancer prevention. Cancer Prev Res (Phila), 3, 985–993.CrossRef Wang, P., Aronson, W. J., Huang, M., et al. (2010). Green tea polyphenols and metabolites in prostatectomy tissue: implications for cancer prevention. Cancer Prev Res (Phila), 3, 985–993.CrossRef
93.
Zurück zum Zitat McLarty, J., Bigelow, R. L., Smith, M., et al. (2009). Tea polyphenols decrease serum levels of prostate-specific antigen, hepatocyte growth factor, and vascular endothelial growth factor in prostate cancer patients and inhibit production of hepatocyte growth factor and vascular endothelial growth factor in vitro. Cancer Prev Res (Phila), 2, 673–682.CrossRef McLarty, J., Bigelow, R. L., Smith, M., et al. (2009). Tea polyphenols decrease serum levels of prostate-specific antigen, hepatocyte growth factor, and vascular endothelial growth factor in prostate cancer patients and inhibit production of hepatocyte growth factor and vascular endothelial growth factor in vitro. Cancer Prev Res (Phila), 2, 673–682.CrossRef
94.
Zurück zum Zitat Mukhopadhyay, A., Bueso-Ramos, C., Chatterjee, D., et al. (2001). Curcumin downregulates cell survival mechanisms in human prostate cancer cell lines. Oncogene, 20, 7597–7609.PubMedCrossRef Mukhopadhyay, A., Bueso-Ramos, C., Chatterjee, D., et al. (2001). Curcumin downregulates cell survival mechanisms in human prostate cancer cell lines. Oncogene, 20, 7597–7609.PubMedCrossRef
95.
Zurück zum Zitat Chaudhary, L. R., & Hruska, K. A. (2003). Inhibition of cell survival signal protein kinase B/Akt by curcumin in human prostate cancer cells. J Cell Biochem, 89, 1–5.PubMedCrossRef Chaudhary, L. R., & Hruska, K. A. (2003). Inhibition of cell survival signal protein kinase B/Akt by curcumin in human prostate cancer cells. J Cell Biochem, 89, 1–5.PubMedCrossRef
96.
Zurück zum Zitat Kumar, A. P., Garcia, G. E., Ghosh, R., et al. (2003). 4-Hydroxy-3-methoxybenzoic acid methyl ester: a curcumin derivative targets Akt/NF kappa B cell survival signaling pathway: potential for prostate cancer management. Neoplasia, 5, 255–266.PubMedCentralPubMedCrossRef Kumar, A. P., Garcia, G. E., Ghosh, R., et al. (2003). 4-Hydroxy-3-methoxybenzoic acid methyl ester: a curcumin derivative targets Akt/NF kappa B cell survival signaling pathway: potential for prostate cancer management. Neoplasia, 5, 255–266.PubMedCentralPubMedCrossRef
97.
Zurück zum Zitat Nakamura, K., Yasunaga, Y., Segawa, T., et al. (2002). Curcumin downregulates AR gene expression and activation in prostate cancer cell lines. Int J Oncol, 21, 825–830.PubMed Nakamura, K., Yasunaga, Y., Segawa, T., et al. (2002). Curcumin downregulates AR gene expression and activation in prostate cancer cell lines. Int J Oncol, 21, 825–830.PubMed
98.
Zurück zum Zitat Tsui, K. H., Feng, T. H., Lin, C. M., et al. (2008). Curcumin blocks the activation of androgen and interlukin-6 on prostate-specific antigen expression in human prostatic carcinoma cells. J Androl, 29, 661–668.PubMedCrossRef Tsui, K. H., Feng, T. H., Lin, C. M., et al. (2008). Curcumin blocks the activation of androgen and interlukin-6 on prostate-specific antigen expression in human prostatic carcinoma cells. J Androl, 29, 661–668.PubMedCrossRef
99.
Zurück zum Zitat Choi, H. Y., Lim, J. E., & Hong, J. H. (2010). Curcumin interrupts the interaction between the androgen receptor and Wnt/beta-catenin signaling pathway in LNCaP prostate cancer cells. Prostate Cancer Prostatic Dis, 13, 343–349.PubMedCrossRef Choi, H. Y., Lim, J. E., & Hong, J. H. (2010). Curcumin interrupts the interaction between the androgen receptor and Wnt/beta-catenin signaling pathway in LNCaP prostate cancer cells. Prostate Cancer Prostatic Dis, 13, 343–349.PubMedCrossRef
100.
Zurück zum Zitat Cabrespine-Faugeras, A., Bayet-Robert, M., Bay, J. O., et al. (2010). Possible benefits of curcumin regimen in combination with taxane chemotherapy for hormone-refractory prostate cancer treatment. Nutr Cancer, 62, 148–153.PubMedCrossRef Cabrespine-Faugeras, A., Bayet-Robert, M., Bay, J. O., et al. (2010). Possible benefits of curcumin regimen in combination with taxane chemotherapy for hormone-refractory prostate cancer treatment. Nutr Cancer, 62, 148–153.PubMedCrossRef
101.
Zurück zum Zitat Deeb, D., Xu, Y. X., Jiang, H., et al. (2003). Curcumin (diferuloyl-methane) enhances tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in LNCaP prostate cancer cells. Mol Cancer Ther, 2, 95–103.PubMedCrossRef Deeb, D., Xu, Y. X., Jiang, H., et al. (2003). Curcumin (diferuloyl-methane) enhances tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis in LNCaP prostate cancer cells. Mol Cancer Ther, 2, 95–103.PubMedCrossRef
102.
Zurück zum Zitat Shankar, S., Ganapathy, S., Chen, Q., et al. (2008). Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis, and angiogenesis. Mol Cancer, 7, 16.PubMedCentralPubMedCrossRef Shankar, S., Ganapathy, S., Chen, Q., et al. (2008). Curcumin sensitizes TRAIL-resistant xenografts: molecular mechanisms of apoptosis, metastasis, and angiogenesis. Mol Cancer, 7, 16.PubMedCentralPubMedCrossRef
103.
Zurück zum Zitat Chendil, D., Ranga, R. S., Meigooni, D., et al. (2004). Curcumin confers radiosensitizing effect in prostate cancer cell line PC-3. Oncogene, 23, 1599–1607.PubMedCrossRef Chendil, D., Ranga, R. S., Meigooni, D., et al. (2004). Curcumin confers radiosensitizing effect in prostate cancer cell line PC-3. Oncogene, 23, 1599–1607.PubMedCrossRef
104.
Zurück zum Zitat Ide, H., Tokiwa, S., Sakamaki, K., et al. (2010). Combined inhibitory effects of soy isoflavones and curcumin on the production of prostate-specific antigen. Prostate, 70, 1127–1133.PubMedCrossRef Ide, H., Tokiwa, S., Sakamaki, K., et al. (2010). Combined inhibitory effects of soy isoflavones and curcumin on the production of prostate-specific antigen. Prostate, 70, 1127–1133.PubMedCrossRef
Metadaten
Titel
Recent progress on nutraceutical research in prostate cancer
verfasst von
Yiwei Li
Aamir Ahmad
Dejuan Kong
Bin Bao
Fazlul H. Sarkar
Publikationsdatum
01.09.2014
Verlag
Springer US
Erschienen in
Cancer and Metastasis Reviews / Ausgabe 2-3/2014
Print ISSN: 0167-7659
Elektronische ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-013-9478-9

Weitere Artikel der Ausgabe 2-3/2014

Cancer and Metastasis Reviews 2-3/2014 Zur Ausgabe

Adjuvante Immuntherapie verlängert Leben bei RCC

25.04.2024 Nierenkarzinom Nachrichten

Nun gibt es auch Resultate zum Gesamtüberleben: Eine adjuvante Pembrolizumab-Therapie konnte in einer Phase-3-Studie das Leben von Menschen mit Nierenzellkarzinom deutlich verlängern. Die Sterberate war im Vergleich zu Placebo um 38% geringer.

Alectinib verbessert krankheitsfreies Überleben bei ALK-positivem NSCLC

25.04.2024 NSCLC Nachrichten

Das Risiko für Rezidiv oder Tod von Patienten und Patientinnen mit reseziertem ALK-positivem NSCLC ist unter einer adjuvanten Therapie mit dem Tyrosinkinase-Inhibitor Alectinib signifikant geringer als unter platinbasierter Chemotherapie.

Bei Senioren mit Prostatakarzinom auf Anämie achten!

24.04.2024 DGIM 2024 Nachrichten

Patienten, die zur Behandlung ihres Prostatakarzinoms eine Androgendeprivationstherapie erhalten, entwickeln nicht selten eine Anämie. Wer ältere Patienten internistisch mitbetreut, sollte auf diese Nebenwirkung achten.

ICI-Therapie in der Schwangerschaft wird gut toleriert

Müssen sich Schwangere einer Krebstherapie unterziehen, rufen Immuncheckpointinhibitoren offenbar nicht mehr unerwünschte Wirkungen hervor als andere Mittel gegen Krebs.

Update Onkologie

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.