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Erschienen in: Journal of Infection and Chemotherapy 3/2012

01.06.2012 | Original Article

Apoptosis of bladder cancer by sodium butyrate and cisplatin

verfasst von: Takuo Maruyama, Shingo Yamamoto, Jun Qiu, Yasuo Ueda, Toru Suzuki, Michio Nojima, Hiroki Shima

Erschienen in: Journal of Infection and Chemotherapy | Ausgabe 3/2012

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Abstract

The effects of sodium butyrate (SB), a histone deacetylase inhibitor, in combination with cisplatin (CDDP), for inhibition of cell growth and induction of apoptosis were investigated in bladder cancer cell lines in vitro. Bladder cancer cell lines T24, 253J, and UMUC3 were treated with different concentrations of CDDP or SB. Cell proliferation was studied by XTT assay. Cell-cycle analysis and induction of apoptosis were analyzed by laser scanning cytometry (LSC). Western blot analysis was used to determine expression of p21, p27, TRADD, FADD, caspase-2, and caspase-7. We observed that SB in combination with CDDP induced significant inhibition of cell growth in a dose-dependent manner through G1 arrest and apoptosis, as determined by LSC. When bladder cancer cell lines were treated with SB plus CDDP, Western blotting showed increased expression of p21 but not p27 in T24 cells, whereas both p21 and p27 increased in 253J and UMUC3 cells. All cell lines exhibited a moderate increase in TRADD and decrease in procaspase-2 but no significant change in FADD and procaspase-7. The results showed the synergistic anticancer effect of SB in combination with CDDP, their potential for treatment of bladder cancer, and their mechanism of action in terms of cell signal transduction and induction of apoptosis.
Literatur
1.
Zurück zum Zitat Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ. Cancer statistics, 2009. CA Cancer J Clin. 2009;59:225–49.PubMedCrossRef Jemal A, Siegel R, Ward E, Hao Y, Xu J, Thun MJ. Cancer statistics, 2009. CA Cancer J Clin. 2009;59:225–49.PubMedCrossRef
2.
Zurück zum Zitat Sawa H, Murakami H, Ohshima Y, Sugino T, Nakajyo T, Kisanuki T, et al. Histone deacetylase inhibitors such as sodium butyrate and trichostatin A induce apoptosis through an increase of the bcl-2-related protein Bad. Brain Tumor Pathol. 2001;18:109–14.PubMedCrossRef Sawa H, Murakami H, Ohshima Y, Sugino T, Nakajyo T, Kisanuki T, et al. Histone deacetylase inhibitors such as sodium butyrate and trichostatin A induce apoptosis through an increase of the bcl-2-related protein Bad. Brain Tumor Pathol. 2001;18:109–14.PubMedCrossRef
3.
Zurück zum Zitat Hernandez A, Thomas R, Smith F, Sandberg J, Kim S, Chung DH, et al. Butyrate sensitizes human colon cancer cells to TRAIL-mediated apoptosis. Surgery (St. Louis). 2001;130:265–72.CrossRef Hernandez A, Thomas R, Smith F, Sandberg J, Kim S, Chung DH, et al. Butyrate sensitizes human colon cancer cells to TRAIL-mediated apoptosis. Surgery (St. Louis). 2001;130:265–72.CrossRef
4.
Zurück zum Zitat Chopin V, Toillon RA, Jouy N, Le Bourhis X. Sodium butyrate induces P53-independent, Fas-mediated apoptosis in MCF-7 human breast cancer cells. Br J Pharmacol. 2002;135:79–86.PubMedCrossRef Chopin V, Toillon RA, Jouy N, Le Bourhis X. Sodium butyrate induces P53-independent, Fas-mediated apoptosis in MCF-7 human breast cancer cells. Br J Pharmacol. 2002;135:79–86.PubMedCrossRef
5.
Zurück zum Zitat Marks P, Rifkind RA, Richon VM, Breslow R, Miller T, Kelly WK. Histone deacetylases and cancer: causes and therapies. Nat Rev Cancer. 2001;1:194–202.PubMedCrossRef Marks P, Rifkind RA, Richon VM, Breslow R, Miller T, Kelly WK. Histone deacetylases and cancer: causes and therapies. Nat Rev Cancer. 2001;1:194–202.PubMedCrossRef
6.
Zurück zum Zitat Marks PA, Richon VM, Breslow R, Rifkind RA. Histone deacetylases inhibitors as new cancer drugs. Curr Opin Oncol. 2001;13:477–83.PubMedCrossRef Marks PA, Richon VM, Breslow R, Rifkind RA. Histone deacetylases inhibitors as new cancer drugs. Curr Opin Oncol. 2001;13:477–83.PubMedCrossRef
7.
Zurück zum Zitat Vigushin DM, Coombes RC. Histone deacetylases inhibitors in cancer treatment. Anticancer Drugs. 2002;13:1–13.PubMedCrossRef Vigushin DM, Coombes RC. Histone deacetylases inhibitors in cancer treatment. Anticancer Drugs. 2002;13:1–13.PubMedCrossRef
8.
9.
Zurück zum Zitat Yoshida M, Horinouchi S, Beppu T. Trichostatin A and trapoxin: novel chemical probes for the role of histone acetylation in chromatin structure and function. Bioessays. 1995;17:423–30.PubMedCrossRef Yoshida M, Horinouchi S, Beppu T. Trichostatin A and trapoxin: novel chemical probes for the role of histone acetylation in chromatin structure and function. Bioessays. 1995;17:423–30.PubMedCrossRef
10.
Zurück zum Zitat Strait KA, Dabbas B, Hammond EH, Warnick CT, Iistrup SJ, Ford CD. Cell cycle blockade and differentiation of ovarian cancer cells by the histone deacetylase inhibitor trichostatin A are associated with changes in p21, Rb, and Id proteins. Mol Cancer Ther. 2002;1:1181–90.PubMed Strait KA, Dabbas B, Hammond EH, Warnick CT, Iistrup SJ, Ford CD. Cell cycle blockade and differentiation of ovarian cancer cells by the histone deacetylase inhibitor trichostatin A are associated with changes in p21, Rb, and Id proteins. Mol Cancer Ther. 2002;1:1181–90.PubMed
11.
Zurück zum Zitat Donadelli M, Costanzo C, Faggioli L, Scupoli MT, Moore PS, Bassi C, et al. Trichostatin A, an inhibitor of histone deacetylases, strongly suppresses growth of pancreatic adenocarcinoma cells. Mol Carcinog. 2003;38:59–69.PubMedCrossRef Donadelli M, Costanzo C, Faggioli L, Scupoli MT, Moore PS, Bassi C, et al. Trichostatin A, an inhibitor of histone deacetylases, strongly suppresses growth of pancreatic adenocarcinoma cells. Mol Carcinog. 2003;38:59–69.PubMedCrossRef
12.
Zurück zum Zitat Chopin V, Toillon RA, Jouy N, Le Bourhis X. P21(WAF1/CIP1) is dispensable for G1 arrest, but indispensable for apoptosis induced by sodium butyrate in MCF-7 breast cancer cells. Oncogene. 2004;23:21–9.PubMedCrossRef Chopin V, Toillon RA, Jouy N, Le Bourhis X. P21(WAF1/CIP1) is dispensable for G1 arrest, but indispensable for apoptosis induced by sodium butyrate in MCF-7 breast cancer cells. Oncogene. 2004;23:21–9.PubMedCrossRef
13.
Zurück zum Zitat Wang ZM, Hu J, Zhou D, Xu ZY, Panasci LC, Chen ZP. Trichostatin A inhibits proliferation and induces expression of P21WAF and p27 in human brain tumor cell lines. Ai Zheng. 2002;21:1100–5.PubMed Wang ZM, Hu J, Zhou D, Xu ZY, Panasci LC, Chen ZP. Trichostatin A inhibits proliferation and induces expression of P21WAF and p27 in human brain tumor cell lines. Ai Zheng. 2002;21:1100–5.PubMed
14.
Zurück zum Zitat Chen Z, Clark S, Birkeland M, Sung CM, Lago A, Liu R, et al. Induction and super-induction of growth arrest and DNA damage 45(GADD45) alpha and beta messenger RNAs by histone deacetylase inhibitors trichostatin A (TSA) and butyrate in SW620 human colon carcinoma cells. Cancer Lett. 2002;188:127–40.PubMedCrossRef Chen Z, Clark S, Birkeland M, Sung CM, Lago A, Liu R, et al. Induction and super-induction of growth arrest and DNA damage 45(GADD45) alpha and beta messenger RNAs by histone deacetylase inhibitors trichostatin A (TSA) and butyrate in SW620 human colon carcinoma cells. Cancer Lett. 2002;188:127–40.PubMedCrossRef
15.
Zurück zum Zitat Kim YB, Ki SW, Yoshida M, Horinouchi S. Mechanism of cell cycle arrest caused by histone deacetylase inhibitors in human carcinoma cells. J Antibiot (Tokyo). 2000;53:1191–200.CrossRef Kim YB, Ki SW, Yoshida M, Horinouchi S. Mechanism of cell cycle arrest caused by histone deacetylase inhibitors in human carcinoma cells. J Antibiot (Tokyo). 2000;53:1191–200.CrossRef
16.
Zurück zum Zitat Li GC, Zhang X, Pan TJ, Chen Z, Ye ZQ. Histone deacetylase inhibitor trichostatin A inhibits the growth of bladder cancer cells through induction of p21WAF1 and G1 cell cycle arrest. Int J Urol. 2006;13:581–6.PubMedCrossRef Li GC, Zhang X, Pan TJ, Chen Z, Ye ZQ. Histone deacetylase inhibitor trichostatin A inhibits the growth of bladder cancer cells through induction of p21WAF1 and G1 cell cycle arrest. Int J Urol. 2006;13:581–6.PubMedCrossRef
17.
Zurück zum Zitat Gould JJ, Kenney PA, Rieger-Christ KM, Silva Neto B, Wszolek MF, LaVoie A, et al. Identification of tumor and invasion suppressor gene modulators in bladder cancer by different classes of histone deacetylase inhibitors using reverse phase protein arrays. J Urol. 2010;183:2395–402.PubMedCrossRef Gould JJ, Kenney PA, Rieger-Christ KM, Silva Neto B, Wszolek MF, LaVoie A, et al. Identification of tumor and invasion suppressor gene modulators in bladder cancer by different classes of histone deacetylase inhibitors using reverse phase protein arrays. J Urol. 2010;183:2395–402.PubMedCrossRef
18.
Zurück zum Zitat Wang D, Wang Z, Tian B, Li X, Li S, Tian Y. Two hour exposure to sodium butyrate sensitizes bladder cancer to anticancer drugs. Int J Urol. 2008;15:435–41.PubMedCrossRef Wang D, Wang Z, Tian B, Li X, Li S, Tian Y. Two hour exposure to sodium butyrate sensitizes bladder cancer to anticancer drugs. Int J Urol. 2008;15:435–41.PubMedCrossRef
19.
Zurück zum Zitat Hara I, Miyake H, Hara S, Arakawa S, Kamidono S. Sodium butyrate induces apoptosis in human renal cell carcinoma cells and synergistically enhances their sensitivity to anti-Fas-mediated cytotoxicity. Int J Oncol. 2000;17:1213–8.PubMed Hara I, Miyake H, Hara S, Arakawa S, Kamidono S. Sodium butyrate induces apoptosis in human renal cell carcinoma cells and synergistically enhances their sensitivity to anti-Fas-mediated cytotoxicity. Int J Oncol. 2000;17:1213–8.PubMed
20.
Zurück zum Zitat Timmermann S, Lehrmann H, Polesskaya A, Harel-Bellan A. Histone acetylation and disease. Cell Mol Life Sci. 2001;58:728–36.PubMedCrossRef Timmermann S, Lehrmann H, Polesskaya A, Harel-Bellan A. Histone acetylation and disease. Cell Mol Life Sci. 2001;58:728–36.PubMedCrossRef
21.
Zurück zum Zitat Qiu J, Yamamoto S, Maruyama T, Kondoh N, Nojima M, Shima H. Growth suppression of prostate cancer cells by sodium butyrate in vitro. Acta Med Hyogo. 2007;32:77–85. Qiu J, Yamamoto S, Maruyama T, Kondoh N, Nojima M, Shima H. Growth suppression of prostate cancer cells by sodium butyrate in vitro. Acta Med Hyogo. 2007;32:77–85.
22.
Zurück zum Zitat Xiong Y, Hannon GJ, Zhang H, Casso D, Kobayashi R, Beach D. p21 is a universal inhibitor of cyclin kinase. Nature (Lond). 1993;366:701–4.CrossRef Xiong Y, Hannon GJ, Zhang H, Casso D, Kobayashi R, Beach D. p21 is a universal inhibitor of cyclin kinase. Nature (Lond). 1993;366:701–4.CrossRef
23.
Zurück zum Zitat Harper JW, Adami GR, Wei N, Keyomarsi K, Elledge SJ. The p21 cdk-interacting protein Cipl is a potent inhibitor of G1 cyclin-dependent kinases. Cell. 1993;75:805–16.PubMedCrossRef Harper JW, Adami GR, Wei N, Keyomarsi K, Elledge SJ. The p21 cdk-interacting protein Cipl is a potent inhibitor of G1 cyclin-dependent kinases. Cell. 1993;75:805–16.PubMedCrossRef
24.
Zurück zum Zitat el-Deiry WS, Tokino T, Velculescu VE, Levy DB, Parsons R, Trent JM, et al. WAF1, a potential mediator of p53 tumor suppression. Cell. 1993;75:817–25.PubMedCrossRef el-Deiry WS, Tokino T, Velculescu VE, Levy DB, Parsons R, Trent JM, et al. WAF1, a potential mediator of p53 tumor suppression. Cell. 1993;75:817–25.PubMedCrossRef
25.
Zurück zum Zitat Lacombe L, Orlow I, Silver D, Gerald WL, Fair WR, Reuter VE, et al. Analysis of p21Waf1/CIP1 in primary bladder tumors. Oncol Res. 1996;8:409–14.PubMed Lacombe L, Orlow I, Silver D, Gerald WL, Fair WR, Reuter VE, et al. Analysis of p21Waf1/CIP1 in primary bladder tumors. Oncol Res. 1996;8:409–14.PubMed
26.
Zurück zum Zitat Richon VM, Sandhoff TW, Rifkind RA, Marks PA. Histone deacetylase inhibitor selectively induces p21WAF1 expression and gene-associated histone acetylation. Proc Natl Acad Sci USA. 2000;97:10014–9.PubMedCrossRef Richon VM, Sandhoff TW, Rifkind RA, Marks PA. Histone deacetylase inhibitor selectively induces p21WAF1 expression and gene-associated histone acetylation. Proc Natl Acad Sci USA. 2000;97:10014–9.PubMedCrossRef
27.
Zurück zum Zitat Hashimoto-Tamaoki T. Control of the cell cycle: cloning and functional analyses of the tumor suppressor genes. Acta Med Hyogo. 2002;27:167–81. Hashimoto-Tamaoki T. Control of the cell cycle: cloning and functional analyses of the tumor suppressor genes. Acta Med Hyogo. 2002;27:167–81.
28.
Zurück zum Zitat Shang D, Liu Y, Matsui Y, Ito N, Nishiyama H, Kamoto T, et al. Demethylating agent 5-aza-2′-deoxycytidine enhances susceptibility of bladder transitional cell carcinoma to cisplatin. Urology. 2008;71:1220–5.PubMedCrossRef Shang D, Liu Y, Matsui Y, Ito N, Nishiyama H, Kamoto T, et al. Demethylating agent 5-aza-2′-deoxycytidine enhances susceptibility of bladder transitional cell carcinoma to cisplatin. Urology. 2008;71:1220–5.PubMedCrossRef
29.
Zurück zum Zitat Rokhlin OW, Bishop GA, Hostager BS, Waldschmidt TJ, Sidorenko SP, Pavloff N, et al. Fas-mediated apoptosis in human prostatic carcinoma cell lines. Cancer Res. 1997;57:1758–68.PubMed Rokhlin OW, Bishop GA, Hostager BS, Waldschmidt TJ, Sidorenko SP, Pavloff N, et al. Fas-mediated apoptosis in human prostatic carcinoma cell lines. Cancer Res. 1997;57:1758–68.PubMed
30.
Zurück zum Zitat Los M, Wesselborg S, Schulze-Osthoff K. The role of caspases in development, immunity, and apoptotic signal transduction: lessons from knockout mice. Immunity. 1999;10:629–39.PubMedCrossRef Los M, Wesselborg S, Schulze-Osthoff K. The role of caspases in development, immunity, and apoptotic signal transduction: lessons from knockout mice. Immunity. 1999;10:629–39.PubMedCrossRef
31.
Zurück zum Zitat McKnight JJ, Gray SB, O’Kane HF, Johnston SR, Williamson KE. Apoptosis and chemotherapy for bladder cancer. J Urol. 2005;173:683–90.PubMedCrossRef McKnight JJ, Gray SB, O’Kane HF, Johnston SR, Williamson KE. Apoptosis and chemotherapy for bladder cancer. J Urol. 2005;173:683–90.PubMedCrossRef
32.
Zurück zum Zitat Wilson NS, Dixit V, Ashkenazi A. Death receptor signal transducers: nodes of coordination in immune signaling networks. Nat Immunol. 2009;10:348–55.PubMedCrossRef Wilson NS, Dixit V, Ashkenazi A. Death receptor signal transducers: nodes of coordination in immune signaling networks. Nat Immunol. 2009;10:348–55.PubMedCrossRef
33.
Zurück zum Zitat Kinoshita H, Yoshikawa H, Shiiki K, Hamada Y, Nakajima Y, Tasaka K. Cisplatin (CDDP) sensitizes human osteosarcoma cell to Fas/CD95-mediated apoptosis by down-regulating FLIP-L expression. Int J Cancer. 2000;88:986–91.PubMedCrossRef Kinoshita H, Yoshikawa H, Shiiki K, Hamada Y, Nakajima Y, Tasaka K. Cisplatin (CDDP) sensitizes human osteosarcoma cell to Fas/CD95-mediated apoptosis by down-regulating FLIP-L expression. Int J Cancer. 2000;88:986–91.PubMedCrossRef
34.
Zurück zum Zitat Ho LH, Taylor R, Dorstyn L, Cakouros D, Bouillet P, Kumar S. A tumor suppressor function for caspase-2. Proc Natl Acad Sci USA. 2009;106:5336–41.PubMedCrossRef Ho LH, Taylor R, Dorstyn L, Cakouros D, Bouillet P, Kumar S. A tumor suppressor function for caspase-2. Proc Natl Acad Sci USA. 2009;106:5336–41.PubMedCrossRef
35.
Zurück zum Zitat Yano T, Itoh Y, Matsuo M, Kawashiri T, Egashira N, Oishi R. Involvement of both tumor necrosis factor-alpha-induced necrosis and p53-mediated caspase-dependent apoptosis in nephrotoxicity of cisplatin. Apoptosis. 2007;12:1901–9.PubMedCrossRef Yano T, Itoh Y, Matsuo M, Kawashiri T, Egashira N, Oishi R. Involvement of both tumor necrosis factor-alpha-induced necrosis and p53-mediated caspase-dependent apoptosis in nephrotoxicity of cisplatin. Apoptosis. 2007;12:1901–9.PubMedCrossRef
36.
Zurück zum Zitat Lin J, Zhang Z, Yang J, Zeng S, Liu BF, Luo Q. Real-time detection of caspase-2 activation in a single living HeLa cell during cisplatin-induced apoptosis. J Biomed Opt. 2006;11:024011.PubMedCrossRef Lin J, Zhang Z, Yang J, Zeng S, Liu BF, Luo Q. Real-time detection of caspase-2 activation in a single living HeLa cell during cisplatin-induced apoptosis. J Biomed Opt. 2006;11:024011.PubMedCrossRef
Metadaten
Titel
Apoptosis of bladder cancer by sodium butyrate and cisplatin
verfasst von
Takuo Maruyama
Shingo Yamamoto
Jun Qiu
Yasuo Ueda
Toru Suzuki
Michio Nojima
Hiroki Shima
Publikationsdatum
01.06.2012
Verlag
Springer Japan
Erschienen in
Journal of Infection and Chemotherapy / Ausgabe 3/2012
Print ISSN: 1341-321X
Elektronische ISSN: 1437-7780
DOI
https://doi.org/10.1007/s10156-011-0322-2

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