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Erschienen in: Cancer and Metastasis Reviews 1/2018

27.12.2017

miR-155 in cancer drug resistance and as target for miRNA-based therapeutics

verfasst von: Recep Bayraktar, Katrien Van Roosbroeck

Erschienen in: Cancer and Metastasis Reviews | Ausgabe 1/2018

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Abstract

Small non-coding microRNAs (miRNAs) are instrumental in physiological processes, such as proliferation, cell cycle, apoptosis, and differentiation, processes which are often disrupted in diseases like cancer. miR-155 is one of the best conserved and multifunctional miRNAs, which is mainly characterized by overexpression in multiple diseases including malignant tumors. Altered expression of miR-155 is found to be associated with various physiological and pathological processes, including hematopoietic lineage differentiation, immune response, inflammation, and tumorigenesis. Furthermore, miR-155 drives therapy resistance mechanisms in various tumor types. Therefore, miR-155-mediated signaling pathways became a potential target for the molecular treatment of cancer. In this review, we summarize the current findings of miR-155 in hematopoietic lineage differentiation, the immune response, inflammation, and cancer therapy resistance. Furthermore, we discuss the potential of miR-155-based therapeutic approaches for the treatment of cancer.
Literatur
2.
Zurück zum Zitat Ha, M., & Kim, V. N. (2014). Regulation of microRNA biogenesis. Nature Reviews. Molecular Cell Biology, 15(8), 509–524.PubMedCrossRef Ha, M., & Kim, V. N. (2014). Regulation of microRNA biogenesis. Nature Reviews. Molecular Cell Biology, 15(8), 509–524.PubMedCrossRef
3.
Zurück zum Zitat Bayraktar, R., et al. (2017). MicroRNA 603 acts as a tumor suppressor and inhibits triple-negative breast cancer tumorigenesis by targeting elongation factor 2 kinase. Oncotarget, 8(7), 11641–11658.PubMedCrossRef Bayraktar, R., et al. (2017). MicroRNA 603 acts as a tumor suppressor and inhibits triple-negative breast cancer tumorigenesis by targeting elongation factor 2 kinase. Oncotarget, 8(7), 11641–11658.PubMedCrossRef
4.
Zurück zum Zitat Kanlikilicer, P., et al. (2016). Ubiquitous release of exosomal tumor suppressor miR-6126 from ovarian cancer cells. Cancer Research, 76(24), 7194–7207.PubMedCrossRef Kanlikilicer, P., et al. (2016). Ubiquitous release of exosomal tumor suppressor miR-6126 from ovarian cancer cells. Cancer Research, 76(24), 7194–7207.PubMedCrossRef
5.
Zurück zum Zitat Mangala, L. S., et al. (2016). Improving vascular maturation using noncoding RNAs increases antitumor effect of chemotherapy. JCI Insight, 1(17), e87754.PubMedPubMedCentralCrossRef Mangala, L. S., et al. (2016). Improving vascular maturation using noncoding RNAs increases antitumor effect of chemotherapy. JCI Insight, 1(17), e87754.PubMedPubMedCentralCrossRef
6.
Zurück zum Zitat Rashed, M. H., et al. (2017). Exosomal miR-940 maintains SRC-mediated oncogenic activity in cancer cells: a possible role for exosomal disposal of tumor suppressor miRNAs. Oncotarget, 8(12), 20145–20164.PubMedPubMedCentralCrossRef Rashed, M. H., et al. (2017). Exosomal miR-940 maintains SRC-mediated oncogenic activity in cancer cells: a possible role for exosomal disposal of tumor suppressor miRNAs. Oncotarget, 8(12), 20145–20164.PubMedPubMedCentralCrossRef
7.
Zurück zum Zitat Bentwich, I., et al. (2005). Identification of hundreds of conserved and nonconserved human microRNAs. Nature Genetics, 37(7), 766–770.PubMedCrossRef Bentwich, I., et al. (2005). Identification of hundreds of conserved and nonconserved human microRNAs. Nature Genetics, 37(7), 766–770.PubMedCrossRef
8.
Zurück zum Zitat Calin, G. A., & Croce, C. M. (2006). MicroRNAs and chromosomal abnormalities in cancer cells. Oncogene, 25(46), 6202–6210.PubMedCrossRef Calin, G. A., & Croce, C. M. (2006). MicroRNAs and chromosomal abnormalities in cancer cells. Oncogene, 25(46), 6202–6210.PubMedCrossRef
9.
Zurück zum Zitat Calin, G. A., et al. (2002). Frequent deletions and down-regulation of micro-RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia. Proceedings of the National Academy of Sciences of the United States of America, 99(24), 15524–15529.PubMedPubMedCentralCrossRef Calin, G. A., et al. (2002). Frequent deletions and down-regulation of micro-RNA genes miR15 and miR16 at 13q14 in chronic lymphocytic leukemia. Proceedings of the National Academy of Sciences of the United States of America, 99(24), 15524–15529.PubMedPubMedCentralCrossRef
10.
Zurück zum Zitat Van Roosbroeck, K., & Calin, G. A. (2016). MicroRNAs in chronic lymphocytic leukemia: miRacle or miRage for prognosis and targeted therapies? Seminars in Oncology, 43(2), 209–214.PubMedPubMedCentralCrossRef Van Roosbroeck, K., & Calin, G. A. (2016). MicroRNAs in chronic lymphocytic leukemia: miRacle or miRage for prognosis and targeted therapies? Seminars in Oncology, 43(2), 209–214.PubMedPubMedCentralCrossRef
11.
Zurück zum Zitat Van Roosbroeck, K., Pollet, J., & Calin, G. A. (2013). miRNAs and long noncoding RNAs as biomarkers in human diseases. Expert Review of Molecular Diagnostics, 13(2), 183–204.PubMedCrossRef Van Roosbroeck, K., Pollet, J., & Calin, G. A. (2013). miRNAs and long noncoding RNAs as biomarkers in human diseases. Expert Review of Molecular Diagnostics, 13(2), 183–204.PubMedCrossRef
12.
Zurück zum Zitat Chen, S., et al. (2015). Host miR155 promotes tumor growth through a myeloid-derived suppressor cell-dependent mechanism. Cancer Research, 75(3), 519–531.PubMedCrossRef Chen, S., et al. (2015). Host miR155 promotes tumor growth through a myeloid-derived suppressor cell-dependent mechanism. Cancer Research, 75(3), 519–531.PubMedCrossRef
13.
Zurück zum Zitat Haasch, D., et al. (2002). T cell activation induces a noncoding RNA transcript sensitive to inhibition by immunosuppressant drugs and encoded by the proto-oncogene, BIC. Cell Immunol, 217(1–2), 78–86.PubMedCrossRef Haasch, D., et al. (2002). T cell activation induces a noncoding RNA transcript sensitive to inhibition by immunosuppressant drugs and encoded by the proto-oncogene, BIC. Cell Immunol, 217(1–2), 78–86.PubMedCrossRef
14.
Zurück zum Zitat Babar, I. A., et al. (2012). Nanoparticle-based therapy in an in vivo microRNA-155 (miR-155)-dependent mouse model of lymphoma. Proceedings of the National Academy of Sciences of the United States of America, 109(26), E1695–E1704.PubMedPubMedCentralCrossRef Babar, I. A., et al. (2012). Nanoparticle-based therapy in an in vivo microRNA-155 (miR-155)-dependent mouse model of lymphoma. Proceedings of the National Academy of Sciences of the United States of America, 109(26), E1695–E1704.PubMedPubMedCentralCrossRef
15.
Zurück zum Zitat Faraoni, I., et al. (2009). miR-155 gene: a typical multifunctional microRNA. Biochimica et Biophysica Acta, 1792(6), 497–505.PubMedCrossRef Faraoni, I., et al. (2009). miR-155 gene: a typical multifunctional microRNA. Biochimica et Biophysica Acta, 1792(6), 497–505.PubMedCrossRef
16.
Zurück zum Zitat Gironella, M., et al. (2007). Tumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development. Proceedings of the National Academy of Sciences of the United States of America, 104(41), 16170–16175.PubMedPubMedCentralCrossRef Gironella, M., et al. (2007). Tumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development. Proceedings of the National Academy of Sciences of the United States of America, 104(41), 16170–16175.PubMedPubMedCentralCrossRef
17.
Zurück zum Zitat Kong, W., et al. (2014). Upregulation of miRNA-155 promotes tumour angiogenesis by targeting VHL and is associated with poor prognosis and triple-negative breast cancer. Oncogene, 33(6), 679–689.PubMedCrossRef Kong, W., et al. (2014). Upregulation of miRNA-155 promotes tumour angiogenesis by targeting VHL and is associated with poor prognosis and triple-negative breast cancer. Oncogene, 33(6), 679–689.PubMedCrossRef
18.
Zurück zum Zitat O’Connell, R. M., et al. (2009). Inositol phosphatase SHIP1 is a primary target of miR-155. Proceedings of the National Academy of Sciences of the United States of America, 106(17), 7113–7118.PubMedPubMedCentralCrossRef O’Connell, R. M., et al. (2009). Inositol phosphatase SHIP1 is a primary target of miR-155. Proceedings of the National Academy of Sciences of the United States of America, 106(17), 7113–7118.PubMedPubMedCentralCrossRef
19.
Zurück zum Zitat Tili, E., Croce, C. M., & Michaille, J. J. (2009). miR-155: on the crosstalk between inflammation and cancer. International Reviews of Immunology, 28(5), 264–284.PubMedCrossRef Tili, E., Croce, C. M., & Michaille, J. J. (2009). miR-155: on the crosstalk between inflammation and cancer. International Reviews of Immunology, 28(5), 264–284.PubMedCrossRef
20.
Zurück zum Zitat Tili, E., et al. (2011). Mutator activity induced by microRNA-155 (miR-155) links inflammation and cancer. Proceedings of the National Academy of Sciences of the United States of America, 108(12), 4908–4913.PubMedPubMedCentralCrossRef Tili, E., et al. (2011). Mutator activity induced by microRNA-155 (miR-155) links inflammation and cancer. Proceedings of the National Academy of Sciences of the United States of America, 108(12), 4908–4913.PubMedPubMedCentralCrossRef
21.
Zurück zum Zitat Van Roosbroeck, K., et al. (2017). Combining anti-Mir-155 with chemotherapy for the treatment of lung cancers. Clinical Cancer Research, 23(11), 2891–2904.PubMedCrossRef Van Roosbroeck, K., et al. (2017). Combining anti-Mir-155 with chemotherapy for the treatment of lung cancers. Clinical Cancer Research, 23(11), 2891–2904.PubMedCrossRef
22.
Zurück zum Zitat Eis, P. S., et al. (2005). Accumulation of miR-155 and BIC RNA in human B cell lymphomas. Proceedings of the National Academy of Sciences of the United States of America, 102(10), 3627–3632.PubMedPubMedCentralCrossRef Eis, P. S., et al. (2005). Accumulation of miR-155 and BIC RNA in human B cell lymphomas. Proceedings of the National Academy of Sciences of the United States of America, 102(10), 3627–3632.PubMedPubMedCentralCrossRef
23.
Zurück zum Zitat Lagos-Quintana, M., et al. (2002). Identification of tissue-specific microRNAs from mouse. Current Biology, 12(9), 735–739.PubMedCrossRef Lagos-Quintana, M., et al. (2002). Identification of tissue-specific microRNAs from mouse. Current Biology, 12(9), 735–739.PubMedCrossRef
24.
Zurück zum Zitat Tam, W. (2001). Identification and characterization of human BIC, a gene on chromosome 21 that encodes a noncoding RNA. Gene, 274(1–2), 157–167.PubMedCrossRef Tam, W. (2001). Identification and characterization of human BIC, a gene on chromosome 21 that encodes a noncoding RNA. Gene, 274(1–2), 157–167.PubMedCrossRef
25.
26.
Zurück zum Zitat Vargova, K., et al. (2011). MYB transcriptionally regulates the miR-155 host gene in chronic lymphocytic leukemia. Blood, 117(14), 3816–3825.PubMedCrossRef Vargova, K., et al. (2011). MYB transcriptionally regulates the miR-155 host gene in chronic lymphocytic leukemia. Blood, 117(14), 3816–3825.PubMedCrossRef
27.
Zurück zum Zitat Zhao, H., et al. (2017). Transforming growth factor beta1/Smad4 signaling affects osteoclast differentiation via regulation of miR-155 expression. Molecules and Cells, 40(3), 211–221.PubMedPubMedCentral Zhao, H., et al. (2017). Transforming growth factor beta1/Smad4 signaling affects osteoclast differentiation via regulation of miR-155 expression. Molecules and Cells, 40(3), 211–221.PubMedPubMedCentral
28.
Zurück zum Zitat Gerloff, D., et al. (2015). NF-kappaB/STAT5/miR-155 network targets PU.1 in FLT3-ITD-driven acute myeloid leukemia. Leukemia, 29(3), 535–547.PubMedCrossRef Gerloff, D., et al. (2015). NF-kappaB/STAT5/miR-155 network targets PU.1 in FLT3-ITD-driven acute myeloid leukemia. Leukemia, 29(3), 535–547.PubMedCrossRef
29.
Zurück zum Zitat Georgantas III, R. W., et al. (2007). CD34+ hematopoietic stem-progenitor cell microRNA expression and function: a circuit diagram of differentiation control. Proceedings of the National Academy of Sciences of the United States of America, 104(8), 2750–2755.PubMedPubMedCentralCrossRef Georgantas III, R. W., et al. (2007). CD34+ hematopoietic stem-progenitor cell microRNA expression and function: a circuit diagram of differentiation control. Proceedings of the National Academy of Sciences of the United States of America, 104(8), 2750–2755.PubMedPubMedCentralCrossRef
30.
Zurück zum Zitat Masaki, S., et al. (2007). Expression patterns of microRNAs 155 and 451 during normal human erythropoiesis. Biochemical and Biophysical Research Communications, 364(3), 509–514.PubMedCrossRef Masaki, S., et al. (2007). Expression patterns of microRNAs 155 and 451 during normal human erythropoiesis. Biochemical and Biophysical Research Communications, 364(3), 509–514.PubMedCrossRef
32.
Zurück zum Zitat Taganov, K. D., et al. (2006). NF-kappaB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. Proceedings of the National Academy of Sciences of the United States of America, 103(33), 12481–12486.PubMedPubMedCentralCrossRef Taganov, K. D., et al. (2006). NF-kappaB-dependent induction of microRNA miR-146, an inhibitor targeted to signaling proteins of innate immune responses. Proceedings of the National Academy of Sciences of the United States of America, 103(33), 12481–12486.PubMedPubMedCentralCrossRef
33.
Zurück zum Zitat O'Connell, R. M., et al. (2007). MicroRNA-155 is induced during the macrophage inflammatory response. Proceedings of the National Academy of Sciences of the United States of America, 104(5), 1604–1609.PubMedPubMedCentralCrossRef O'Connell, R. M., et al. (2007). MicroRNA-155 is induced during the macrophage inflammatory response. Proceedings of the National Academy of Sciences of the United States of America, 104(5), 1604–1609.PubMedPubMedCentralCrossRef
34.
Zurück zum Zitat Kurowska-Stolarska, M., et al. (2011). MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis. Proceedings of the National Academy of Sciences of the United States of America, 108(27), 11193–11198.PubMedPubMedCentralCrossRef Kurowska-Stolarska, M., et al. (2011). MicroRNA-155 as a proinflammatory regulator in clinical and experimental arthritis. Proceedings of the National Academy of Sciences of the United States of America, 108(27), 11193–11198.PubMedPubMedCentralCrossRef
35.
Zurück zum Zitat Jin, H. M., et al. (2014). MicroRNA-155 as a proinflammatory regulator via SHIP-1 down-regulation in acute gouty arthritis. Arthritis Research & Therapy, 16(2), R88.CrossRef Jin, H. M., et al. (2014). MicroRNA-155 as a proinflammatory regulator via SHIP-1 down-regulation in acute gouty arthritis. Arthritis Research & Therapy, 16(2), R88.CrossRef
36.
Zurück zum Zitat Keir, M. E., et al. (2008). PD-1 and its ligands in tolerance and immunity. Annual Review of Immunology, 26, 677–704.PubMedCrossRef Keir, M. E., et al. (2008). PD-1 and its ligands in tolerance and immunity. Annual Review of Immunology, 26, 677–704.PubMedCrossRef
37.
Zurück zum Zitat Herbst, R. S., et al. (2014). Predictive correlates of response to the anti-PD-L1 antibody MPDL3280A in cancer patients. Nature, 515(7528), 563–567.PubMedPubMedCentralCrossRef Herbst, R. S., et al. (2014). Predictive correlates of response to the anti-PD-L1 antibody MPDL3280A in cancer patients. Nature, 515(7528), 563–567.PubMedPubMedCentralCrossRef
38.
Zurück zum Zitat Powles, T., et al. (2014). MPDL3280A (anti-PD-L1) treatment leads to clinical activity in metastatic bladder cancer. Nature, 515(7528), 558–562.PubMedCrossRef Powles, T., et al. (2014). MPDL3280A (anti-PD-L1) treatment leads to clinical activity in metastatic bladder cancer. Nature, 515(7528), 558–562.PubMedCrossRef
39.
Zurück zum Zitat Yee, D., et al. (2017). MicroRNA-155 induction via TNF-alpha and IFN-gamma suppresses expression of programmed death ligand-1 (PD-L1) in human primary cells. The Journal of Biological Chemistry, 292(50), 20683–20693. Yee, D., et al. (2017). MicroRNA-155 induction via TNF-alpha and IFN-gamma suppresses expression of programmed death ligand-1 (PD-L1) in human primary cells. The Journal of Biological Chemistry, 292(50), 20683–20693.
41.
42.
Zurück zum Zitat Lu, L. F., et al. (2009). Foxp3-dependent microRNA155 confers competitive fitness to regulatory T cells by targeting SOCS1 protein. Immunity, 30(1), 80–91.PubMedPubMedCentralCrossRef Lu, L. F., et al. (2009). Foxp3-dependent microRNA155 confers competitive fitness to regulatory T cells by targeting SOCS1 protein. Immunity, 30(1), 80–91.PubMedPubMedCentralCrossRef
43.
Zurück zum Zitat Yang, L., et al. (2017). MiRNA-155 promotes proliferation by targeting caudal-type homeobox 1 (CDX1) in glioma cells. Biomedicine & Pharmacotherapy, 95, 1759–1764.CrossRef Yang, L., et al. (2017). MiRNA-155 promotes proliferation by targeting caudal-type homeobox 1 (CDX1) in glioma cells. Biomedicine & Pharmacotherapy, 95, 1759–1764.CrossRef
44.
Zurück zum Zitat Liu, Q., et al. (2015). miR-155 regulates glioma cells invasion and chemosensitivity by p38 Isforms in vitro. Journal of Cellular Biochemistry, 116(7), 1213–1221.PubMedCrossRef Liu, Q., et al. (2015). miR-155 regulates glioma cells invasion and chemosensitivity by p38 Isforms in vitro. Journal of Cellular Biochemistry, 116(7), 1213–1221.PubMedCrossRef
45.
Zurück zum Zitat D'Urso, P. I., et al. (2012). miR-155 is up-regulated in primary and secondary glioblastoma and promotes tumour growth by inhibiting GABA receptors. International Journal of Oncology, 41(1), 228–234.PubMed D'Urso, P. I., et al. (2012). miR-155 is up-regulated in primary and secondary glioblastoma and promotes tumour growth by inhibiting GABA receptors. International Journal of Oncology, 41(1), 228–234.PubMed
46.
Zurück zum Zitat Xue, X., et al. (2016). MiR-21 and MiR-155 promote non-small cell lung cancer progression by downregulating SOCS1, SOCS6, and PTEN. Oncotarget, 7(51), 84508–84519.PubMedPubMedCentralCrossRef Xue, X., et al. (2016). MiR-21 and MiR-155 promote non-small cell lung cancer progression by downregulating SOCS1, SOCS6, and PTEN. Oncotarget, 7(51), 84508–84519.PubMedPubMedCentralCrossRef
47.
Zurück zum Zitat Liu, F., et al. (2017). MiR-155 inhibits proliferation and invasion by directly targeting PDCD4 in non-small cell lung cancer. Thorac Cancer, 8(6), 613–619.PubMedPubMedCentralCrossRef Liu, F., et al. (2017). MiR-155 inhibits proliferation and invasion by directly targeting PDCD4 in non-small cell lung cancer. Thorac Cancer, 8(6), 613–619.PubMedPubMedCentralCrossRef
48.
Zurück zum Zitat Al-Haidari, A. A., Syk, I., & Thorlacius, H. (2017). MiR-155-5p positively regulates CCL17-induced colon cancer cell migration by targeting RhoA. Oncotarget, 8(9), 14887–14896.PubMedPubMedCentralCrossRef Al-Haidari, A. A., Syk, I., & Thorlacius, H. (2017). MiR-155-5p positively regulates CCL17-induced colon cancer cell migration by targeting RhoA. Oncotarget, 8(9), 14887–14896.PubMedPubMedCentralCrossRef
49.
Zurück zum Zitat Li, T., et al. (2014). miR-155 regulates the proliferation and cell cycle of colorectal carcinoma cells by targeting E2F2. Biotechnology Letters, 36(9), 1743–1752.PubMedCrossRef Li, T., et al. (2014). miR-155 regulates the proliferation and cell cycle of colorectal carcinoma cells by targeting E2F2. Biotechnology Letters, 36(9), 1743–1752.PubMedCrossRef
50.
Zurück zum Zitat Fu, X., et al. (2017). MicroRNA-155-5p promotes hepatocellular carcinoma progression by suppressing PTEN through the PI3K/Akt pathway. Cancer Science, 108(4), 620–631.PubMedPubMedCentralCrossRef Fu, X., et al. (2017). MicroRNA-155-5p promotes hepatocellular carcinoma progression by suppressing PTEN through the PI3K/Akt pathway. Cancer Science, 108(4), 620–631.PubMedPubMedCentralCrossRef
51.
Zurück zum Zitat Xie, Q., et al. (2012). Aberrant expression of microRNA 155 may accelerate cell proliferation by targeting sex-determining region Y box 6 in hepatocellular carcinoma. Cancer, 118(9), 2431–2442.PubMedCrossRef Xie, Q., et al. (2012). Aberrant expression of microRNA 155 may accelerate cell proliferation by targeting sex-determining region Y box 6 in hepatocellular carcinoma. Cancer, 118(9), 2431–2442.PubMedCrossRef
52.
Zurück zum Zitat Liu, F., et al. (2015). MiR-155 targets TP53INP1 to regulate liver cancer stem cell acquisition and self-renewal. FEBS Letters, 589(4), 500–506.PubMedCrossRef Liu, F., et al. (2015). MiR-155 targets TP53INP1 to regulate liver cancer stem cell acquisition and self-renewal. FEBS Letters, 589(4), 500–506.PubMedCrossRef
53.
Zurück zum Zitat Xiang, X., et al. (2011). miR-155 promotes macroscopic tumor formation yet inhibits tumor dissemination from mammary fat pads to the lung by preventing EMT. Oncogene, 30(31), 3440–3453.PubMedPubMedCentralCrossRef Xiang, X., et al. (2011). miR-155 promotes macroscopic tumor formation yet inhibits tumor dissemination from mammary fat pads to the lung by preventing EMT. Oncogene, 30(31), 3440–3453.PubMedPubMedCentralCrossRef
54.
Zurück zum Zitat Jiang, S., et al. (2010). MicroRNA-155 functions as an OncomiR in breast cancer by targeting the suppressor of cytokine signaling 1 gene. Cancer Research, 70(8), 3119–3127.PubMedCrossRef Jiang, S., et al. (2010). MicroRNA-155 functions as an OncomiR in breast cancer by targeting the suppressor of cytokine signaling 1 gene. Cancer Research, 70(8), 3119–3127.PubMedCrossRef
55.
Zurück zum Zitat Shen, R., et al. (2015). MiRNA-155 mediates TAM resistance by modulating SOCS6-STAT3 signalling pathway in breast cancer. American Journal of Translational Research, 7(10), 2115–2126.PubMedPubMedCentral Shen, R., et al. (2015). MiRNA-155 mediates TAM resistance by modulating SOCS6-STAT3 signalling pathway in breast cancer. American Journal of Translational Research, 7(10), 2115–2126.PubMedPubMedCentral
56.
Zurück zum Zitat Dinami, R., et al. (2014). miR-155 drives telomere fragility in human breast cancer by targeting TRF1. Cancer Research, 74(15), 4145–4156.PubMedCrossRef Dinami, R., et al. (2014). miR-155 drives telomere fragility in human breast cancer by targeting TRF1. Cancer Research, 74(15), 4145–4156.PubMedCrossRef
57.
Zurück zum Zitat Tiago, D. M., et al. (2016). Matrix Gla protein repression by miR-155 promotes oncogenic signals in breast cancer MCF-7 cells. FEBS Letters, 590(8), 1234–1241.PubMedCrossRef Tiago, D. M., et al. (2016). Matrix Gla protein repression by miR-155 promotes oncogenic signals in breast cancer MCF-7 cells. FEBS Letters, 590(8), 1234–1241.PubMedCrossRef
58.
Zurück zum Zitat Bhattacharya, S., et al. (2016). Increased miR-155-5p and reduced miR-148a-3p contribute to the suppression of osteosarcoma cell death. Oncogene, 35(40), 5282–5294.PubMedCrossRef Bhattacharya, S., et al. (2016). Increased miR-155-5p and reduced miR-148a-3p contribute to the suppression of osteosarcoma cell death. Oncogene, 35(40), 5282–5294.PubMedCrossRef
59.
Zurück zum Zitat Rather, M. I., et al. (2013). Oncogenic microRNA-155 down-regulates tumor suppressor CDC73 and promotes oral squamous cell carcinoma cell proliferation: implications for cancer therapeutics. The Journal of Biological Chemistry, 288(1), 608–618.PubMedCrossRef Rather, M. I., et al. (2013). Oncogenic microRNA-155 down-regulates tumor suppressor CDC73 and promotes oral squamous cell carcinoma cell proliferation: implications for cancer therapeutics. The Journal of Biological Chemistry, 288(1), 608–618.PubMedCrossRef
60.
61.
Zurück zum Zitat Sandhu, S. K., et al. (2012). miR-155 targets histone deacetylase 4 (HDAC4) and impairs transcriptional activity of B-cell lymphoma 6 (BCL6) in the Emu-miR-155 transgenic mouse model. Proceedings of the National Academy of Sciences of the United States of America, 109(49), 20047–20052.PubMedPubMedCentralCrossRef Sandhu, S. K., et al. (2012). miR-155 targets histone deacetylase 4 (HDAC4) and impairs transcriptional activity of B-cell lymphoma 6 (BCL6) in the Emu-miR-155 transgenic mouse model. Proceedings of the National Academy of Sciences of the United States of America, 109(49), 20047–20052.PubMedPubMedCentralCrossRef
62.
Zurück zum Zitat Huang, X., et al. (2012). Quantitative proteomics reveals that miR-155 regulates the PI3K-AKT pathway in diffuse large B-cell lymphoma. The American Journal of Pathology, 181(1), 26–33.PubMedPubMedCentralCrossRef Huang, X., et al. (2012). Quantitative proteomics reveals that miR-155 regulates the PI3K-AKT pathway in diffuse large B-cell lymphoma. The American Journal of Pathology, 181(1), 26–33.PubMedPubMedCentralCrossRef
63.
Zurück zum Zitat Pedersen, I. M., et al. (2009). Onco-miR-155 targets SHIP1 to promote TNFalpha-dependent growth of B cell lymphomas. EMBO Molecular Medicine, 1(5), 288–295.PubMedPubMedCentralCrossRef Pedersen, I. M., et al. (2009). Onco-miR-155 targets SHIP1 to promote TNFalpha-dependent growth of B cell lymphomas. EMBO Molecular Medicine, 1(5), 288–295.PubMedPubMedCentralCrossRef
64.
Zurück zum Zitat Willimott, S., & Wagner, S. D. (2012). miR-125b and miR-155 contribute to BCL2 repression and proliferation in response to CD40 ligand (CD154) in human leukemic B-cells. The Journal of Biological Chemistry, 287(4), 2608–2617.PubMedCrossRef Willimott, S., & Wagner, S. D. (2012). miR-125b and miR-155 contribute to BCL2 repression and proliferation in response to CD40 ligand (CD154) in human leukemic B-cells. The Journal of Biological Chemistry, 287(4), 2608–2617.PubMedCrossRef
65.
Zurück zum Zitat Costinean, S., et al. (2009). Src homology 2 domain-containing inositol-5-phosphatase and CCAAT enhancer-binding protein beta are targeted by miR-155 in B cells of Emicro-MiR-155 transgenic mice. Blood, 114(7), 1374–1382.PubMedPubMedCentralCrossRef Costinean, S., et al. (2009). Src homology 2 domain-containing inositol-5-phosphatase and CCAAT enhancer-binding protein beta are targeted by miR-155 in B cells of Emicro-MiR-155 transgenic mice. Blood, 114(7), 1374–1382.PubMedPubMedCentralCrossRef
67.
Zurück zum Zitat Merkel, O., et al. (2015). Oncogenic role of miR-155 in anaplastic large cell lymphoma lacking the t(2;5) translocation. The Journal of Pathology, 236(4), 445–456.PubMedPubMedCentralCrossRef Merkel, O., et al. (2015). Oncogenic role of miR-155 in anaplastic large cell lymphoma lacking the t(2;5) translocation. The Journal of Pathology, 236(4), 445–456.PubMedPubMedCentralCrossRef
68.
Zurück zum Zitat Lawrie, C. H., et al. (2007). MicroRNA expression distinguishes between germinal center B cell-like and activated B cell-like subtypes of diffuse large B cell lymphoma. International Journal of Cancer, 121(5), 1156–1161.PubMedCrossRef Lawrie, C. H., et al. (2007). MicroRNA expression distinguishes between germinal center B cell-like and activated B cell-like subtypes of diffuse large B cell lymphoma. International Journal of Cancer, 121(5), 1156–1161.PubMedCrossRef
69.
Zurück zum Zitat Fulci, V., et al. (2007). Quantitative technologies establish a novel microRNA profile of chronic lymphocytic leukemia. Blood, 109(11), 4944–4951.PubMedCrossRef Fulci, V., et al. (2007). Quantitative technologies establish a novel microRNA profile of chronic lymphocytic leukemia. Blood, 109(11), 4944–4951.PubMedCrossRef
70.
Zurück zum Zitat Kluiver, J., et al. (2005). BIC and miR-155 are highly expressed in Hodgkin, primary mediastinal and diffuse large B cell lymphomas. The Journal of Pathology, 207(2), 243–249.PubMedCrossRef Kluiver, J., et al. (2005). BIC and miR-155 are highly expressed in Hodgkin, primary mediastinal and diffuse large B cell lymphomas. The Journal of Pathology, 207(2), 243–249.PubMedCrossRef
71.
Zurück zum Zitat Faraoni, I., et al. (2012). MiR-424 and miR-155 deregulated expression in cytogenetically normal acute myeloid leukaemia: correlation with NPM1 and FLT3 mutation status. Journal of Hematology & Oncology, 5, 26.CrossRef Faraoni, I., et al. (2012). MiR-424 and miR-155 deregulated expression in cytogenetically normal acute myeloid leukaemia: correlation with NPM1 and FLT3 mutation status. Journal of Hematology & Oncology, 5, 26.CrossRef
72.
Zurück zum Zitat Costinean, S., et al. (2006). Pre-B cell proliferation and lymphoblastic leukemia/high-grade lymphoma in E(mu)-miR155 transgenic mice. Proceedings of the National Academy of Sciences of the United States of America, 103(18), 7024–7029.PubMedPubMedCentralCrossRef Costinean, S., et al. (2006). Pre-B cell proliferation and lymphoblastic leukemia/high-grade lymphoma in E(mu)-miR155 transgenic mice. Proceedings of the National Academy of Sciences of the United States of America, 103(18), 7024–7029.PubMedPubMedCentralCrossRef
73.
Zurück zum Zitat Rosenbauer, F., & Tenen, D. G. (2007). Transcription factors in myeloid development: balancing differentiation with transformation. Nature Reviews. Immunology, 7(2), 105–117.PubMedCrossRef Rosenbauer, F., & Tenen, D. G. (2007). Transcription factors in myeloid development: balancing differentiation with transformation. Nature Reviews. Immunology, 7(2), 105–117.PubMedCrossRef
74.
Zurück zum Zitat Cui, B., et al. (2014). MicroRNA-155 influences B-cell receptor signaling and associates with aggressive disease in chronic lymphocytic leukemia. Blood, 124(4), 546–554.PubMedPubMedCentralCrossRef Cui, B., et al. (2014). MicroRNA-155 influences B-cell receptor signaling and associates with aggressive disease in chronic lymphocytic leukemia. Blood, 124(4), 546–554.PubMedPubMedCentralCrossRef
75.
Zurück zum Zitat Ferrajoli, A., et al. (2013). Prognostic value of miR-155 in individuals with monoclonal B-cell lymphocytosis and patients with B chronic lymphocytic leukemia. Blood, 122(11), 1891–1899.PubMedPubMedCentralCrossRef Ferrajoli, A., et al. (2013). Prognostic value of miR-155 in individuals with monoclonal B-cell lymphocytosis and patients with B chronic lymphocytic leukemia. Blood, 122(11), 1891–1899.PubMedPubMedCentralCrossRef
76.
Zurück zum Zitat Gatto, G., et al. (2008). Epstein-Barr virus latent membrane protein 1 trans-activates miR-155 transcription through the NF-kappaB pathway. Nucleic Acids Research, 36(20), 6608–6619.PubMedPubMedCentralCrossRef Gatto, G., et al. (2008). Epstein-Barr virus latent membrane protein 1 trans-activates miR-155 transcription through the NF-kappaB pathway. Nucleic Acids Research, 36(20), 6608–6619.PubMedPubMedCentralCrossRef
77.
Zurück zum Zitat Lu, F., et al. (2008). Epstein-Barr virus-induced miR-155 attenuates NF-kappaB signaling and stabilizes latent virus persistence. Journal of Virology, 82(21), 10436–10443.PubMedPubMedCentralCrossRef Lu, F., et al. (2008). Epstein-Barr virus-induced miR-155 attenuates NF-kappaB signaling and stabilizes latent virus persistence. Journal of Virology, 82(21), 10436–10443.PubMedPubMedCentralCrossRef
78.
Zurück zum Zitat Kluiver, J., et al. (2007). Regulation of pri-microRNA BIC transcription and processing in Burkitt lymphoma. Oncogene, 26(26), 3769–3776.PubMedCrossRef Kluiver, J., et al. (2007). Regulation of pri-microRNA BIC transcription and processing in Burkitt lymphoma. Oncogene, 26(26), 3769–3776.PubMedCrossRef
79.
Zurück zum Zitat Garzon, R., et al. (2008). Distinctive microRNA signature of acute myeloid leukemia bearing cytoplasmic mutated nucleophosmin. Proceedings of the National Academy of Sciences of the United States of America, 105(10), 3945–3950.PubMedPubMedCentralCrossRef Garzon, R., et al. (2008). Distinctive microRNA signature of acute myeloid leukemia bearing cytoplasmic mutated nucleophosmin. Proceedings of the National Academy of Sciences of the United States of America, 105(10), 3945–3950.PubMedPubMedCentralCrossRef
80.
Zurück zum Zitat Salemi, D., et al. (2015). miR-155 regulative network in FLT3 mutated acute myeloid leukemia. Leukemia Research, 39(8), 883–896.PubMedCrossRef Salemi, D., et al. (2015). miR-155 regulative network in FLT3 mutated acute myeloid leukemia. Leukemia Research, 39(8), 883–896.PubMedCrossRef
81.
Zurück zum Zitat Wallace, J. A., et al. (2017). miR-155 promotes FLT3-ITD-induced myeloproliferative disease through inhibition of the interferon response. Blood, 129(23), 3074–3086.PubMedPubMedCentralCrossRef Wallace, J. A., et al. (2017). miR-155 promotes FLT3-ITD-induced myeloproliferative disease through inhibition of the interferon response. Blood, 129(23), 3074–3086.PubMedPubMedCentralCrossRef
82.
Zurück zum Zitat Palma, C. A., et al. (2014). MicroRNA-155 as an inducer of apoptosis and cell differentiation in acute myeloid leukaemia. Molecular Cancer, 13, 79.PubMedPubMedCentralCrossRef Palma, C. A., et al. (2014). MicroRNA-155 as an inducer of apoptosis and cell differentiation in acute myeloid leukaemia. Molecular Cancer, 13, 79.PubMedPubMedCentralCrossRef
83.
Zurück zum Zitat Narayan, N., et al. (2017). Functionally distinct roles for different miR-155 expression levels through contrasting effects on gene expression, in acute myeloid leukaemia. Leukemia, 31(4), 808–820.PubMedCrossRef Narayan, N., et al. (2017). Functionally distinct roles for different miR-155 expression levels through contrasting effects on gene expression, in acute myeloid leukaemia. Leukemia, 31(4), 808–820.PubMedCrossRef
84.
Zurück zum Zitat Volinia, S., et al. (2006). A microRNA expression signature of human solid tumors defines cancer gene targets. Proceedings of the National Academy of Sciences of the United States of America, 103(7), 2257–2261.PubMedPubMedCentralCrossRef Volinia, S., et al. (2006). A microRNA expression signature of human solid tumors defines cancer gene targets. Proceedings of the National Academy of Sciences of the United States of America, 103(7), 2257–2261.PubMedPubMedCentralCrossRef
85.
Zurück zum Zitat Zhu, M., et al. (2011). Integrated miRNA and mRNA expression profiling of mouse mammary tumor models identifies miRNA signatures associated with mammary tumor lineage. Genome Biology, 12(8), R77.PubMedPubMedCentralCrossRef Zhu, M., et al. (2011). Integrated miRNA and mRNA expression profiling of mouse mammary tumor models identifies miRNA signatures associated with mammary tumor lineage. Genome Biology, 12(8), R77.PubMedPubMedCentralCrossRef
86.
Zurück zum Zitat Neilsen, P. M., et al. (2013). Mutant p53 drives invasion in breast tumors through up-regulation of miR-155. Oncogene, 32(24), 2992–3000.PubMedCrossRef Neilsen, P. M., et al. (2013). Mutant p53 drives invasion in breast tumors through up-regulation of miR-155. Oncogene, 32(24), 2992–3000.PubMedCrossRef
87.
Zurück zum Zitat Johansson, J., et al. (2013). MiR-155-mediated loss of C/EBPbeta shifts the TGF-beta response from growth inhibition to epithelial-mesenchymal transition, invasion and metastasis in breast cancer. Oncogene, 32(50), 5614–5624.PubMedPubMedCentralCrossRef Johansson, J., et al. (2013). MiR-155-mediated loss of C/EBPbeta shifts the TGF-beta response from growth inhibition to epithelial-mesenchymal transition, invasion and metastasis in breast cancer. Oncogene, 32(50), 5614–5624.PubMedPubMedCentralCrossRef
88.
Zurück zum Zitat Yanaihara, N., et al. (2006). Unique microRNA molecular profiles in lung cancer diagnosis and prognosis. Cancer Cell, 9(3), 189–198.PubMedCrossRef Yanaihara, N., et al. (2006). Unique microRNA molecular profiles in lung cancer diagnosis and prognosis. Cancer Cell, 9(3), 189–198.PubMedCrossRef
89.
Zurück zum Zitat Zang, Y. S., et al. (2012). MiR-155 inhibits the sensitivity of lung cancer cells to cisplatin via negative regulation of Apaf-1 expression. Cancer Gene Therapy, 19(11), 773–778.PubMedCrossRef Zang, Y. S., et al. (2012). MiR-155 inhibits the sensitivity of lung cancer cells to cisplatin via negative regulation of Apaf-1 expression. Cancer Gene Therapy, 19(11), 773–778.PubMedCrossRef
90.
Zurück zum Zitat Pouliot, L. M., et al. (2012). Cisplatin sensitivity mediated by WEE1 and CHK1 is mediated by miR-155 and the miR-15 family. Cancer Research, 72(22), 5945–5955.PubMedPubMedCentralCrossRef Pouliot, L. M., et al. (2012). Cisplatin sensitivity mediated by WEE1 and CHK1 is mediated by miR-155 and the miR-15 family. Cancer Research, 72(22), 5945–5955.PubMedPubMedCentralCrossRef
91.
Zurück zum Zitat Kong, W., et al. (2010). MicroRNA-155 regulates cell survival, growth, and chemosensitivity by targeting FOXO3a in breast cancer. The Journal of Biological Chemistry, 285(23), 17869–17879.PubMedPubMedCentralCrossRef Kong, W., et al. (2010). MicroRNA-155 regulates cell survival, growth, and chemosensitivity by targeting FOXO3a in breast cancer. The Journal of Biological Chemistry, 285(23), 17869–17879.PubMedPubMedCentralCrossRef
92.
Zurück zum Zitat Lei, C., et al. (2012). Up-regulated miR155 reverses the epithelial-mesenchymal transition induced by EGF and increases chemo-sensitivity to cisplatin in human Caski cervical cancer cells. PLoS One, 7(12), e52310.PubMedPubMedCentralCrossRef Lei, C., et al. (2012). Up-regulated miR155 reverses the epithelial-mesenchymal transition induced by EGF and increases chemo-sensitivity to cisplatin in human Caski cervical cancer cells. PLoS One, 7(12), e52310.PubMedPubMedCentralCrossRef
93.
Zurück zum Zitat Lv, L., et al. (2016). Effect of miR-155 knockdown on the reversal of doxorubicin resistance in human lung cancer A549/dox cells. Oncology Letters, 11(2), 1161–1166.PubMedCrossRef Lv, L., et al. (2016). Effect of miR-155 knockdown on the reversal of doxorubicin resistance in human lung cancer A549/dox cells. Oncology Letters, 11(2), 1161–1166.PubMedCrossRef
94.
Zurück zum Zitat Li, B., et al. (2017). Morin promotes prostate cancer cells chemosensitivity to paclitaxel through miR-155/GATA3 axis. Oncotarget, 8(29), 47849–47860.PubMedPubMedCentral Li, B., et al. (2017). Morin promotes prostate cancer cells chemosensitivity to paclitaxel through miR-155/GATA3 axis. Oncotarget, 8(29), 47849–47860.PubMedPubMedCentral
95.
Zurück zum Zitat Gu, S., et al. (2017). miR-155 mediates arsenic trioxide resistance by activating Nrf2 and suppressing apoptosis in lung cancer cells. Sci Rep, 7(1), 12155.PubMedPubMedCentralCrossRef Gu, S., et al. (2017). miR-155 mediates arsenic trioxide resistance by activating Nrf2 and suppressing apoptosis in lung cancer cells. Sci Rep, 7(1), 12155.PubMedPubMedCentralCrossRef
96.
Zurück zum Zitat Babar, I. A., et al. (2011). Inhibition of hypoxia-induced miR-155 radiosensitizes hypoxic lung cancer cells. Cancer Biology & Therapy, 12(10), 908–914.CrossRef Babar, I. A., et al. (2011). Inhibition of hypoxia-induced miR-155 radiosensitizes hypoxic lung cancer cells. Cancer Biology & Therapy, 12(10), 908–914.CrossRef
97.
Zurück zum Zitat Khoshinani, H. M., et al. (2017). Involvement of miR-155/FOXO3a and miR-222/PTEN in acquired radioresistance of colorectal cancer cell line. Japanese Journal of Radiology, 35(11), 664–672.PubMedCrossRef Khoshinani, H. M., et al. (2017). Involvement of miR-155/FOXO3a and miR-222/PTEN in acquired radioresistance of colorectal cancer cell line. Japanese Journal of Radiology, 35(11), 664–672.PubMedCrossRef
98.
Zurück zum Zitat Lv, X., et al. (2016). Inhibition of microRNA-155 sensitizes lung cancer cells to irradiation via suppression of HK2-modulated glucose metabolism. Molecular Medicine Reports, 14(2), 1332–1338.PubMedCrossRef Lv, X., et al. (2016). Inhibition of microRNA-155 sensitizes lung cancer cells to irradiation via suppression of HK2-modulated glucose metabolism. Molecular Medicine Reports, 14(2), 1332–1338.PubMedCrossRef
99.
Zurück zum Zitat Yang, F., Liu, Q., & Hu, C. M. (2015). Epstein-Barr virus-encoded LMP1 increases miR-155 expression, which promotes radioresistance of nasopharyngeal carcinoma via suppressing UBQLN1. European Review for Medical and Pharmacological Sciences, 19(23), 4507–4515.PubMed Yang, F., Liu, Q., & Hu, C. M. (2015). Epstein-Barr virus-encoded LMP1 increases miR-155 expression, which promotes radioresistance of nasopharyngeal carcinoma via suppressing UBQLN1. European Review for Medical and Pharmacological Sciences, 19(23), 4507–4515.PubMed
100.
Zurück zum Zitat Gasparini, P., et al. (2014). Protective role of miR-155 in breast cancer through RAD51 targeting impairs homologous recombination after irradiation. Proceedings of the National Academy of Sciences of the United States of America, 111(12), 4536–4541.PubMedPubMedCentralCrossRef Gasparini, P., et al. (2014). Protective role of miR-155 in breast cancer through RAD51 targeting impairs homologous recombination after irradiation. Proceedings of the National Academy of Sciences of the United States of America, 111(12), 4536–4541.PubMedPubMedCentralCrossRef
101.
Zurück zum Zitat Narita, M., et al. (2017). Chronic treatment of non-small-cell lung cancer cells with gefitinib leads to an epigenetic loss of epithelial properties associated with reductions in microRNA-155 and -200c. PLoS One, 12(2), e0172115.PubMedPubMedCentralCrossRef Narita, M., et al. (2017). Chronic treatment of non-small-cell lung cancer cells with gefitinib leads to an epigenetic loss of epithelial properties associated with reductions in microRNA-155 and -200c. PLoS One, 12(2), e0172115.PubMedPubMedCentralCrossRef
102.
Zurück zum Zitat Chiu, C. F., et al. (2016). NF-kappaB-driven suppression of FOXO3a contributes to EGFR mutation-independent gefitinib resistance. Proceedings of the National Academy of Sciences of the United States of America, 113(18), E2526–E2535.PubMedPubMedCentralCrossRef Chiu, C. F., et al. (2016). NF-kappaB-driven suppression of FOXO3a contributes to EGFR mutation-independent gefitinib resistance. Proceedings of the National Academy of Sciences of the United States of America, 113(18), E2526–E2535.PubMedPubMedCentralCrossRef
103.
Zurück zum Zitat Kim, J. H., Kim, W. S., & Park, C. (2012). Epstein-Barr virus latent membrane protein-1 protects B-cell lymphoma from rituximab-induced apoptosis through miR-155-mediated Akt activation and up-regulation of Mcl-1. Leukemia & Lymphoma, 53(8), 1586–1591.CrossRef Kim, J. H., Kim, W. S., & Park, C. (2012). Epstein-Barr virus latent membrane protein-1 protects B-cell lymphoma from rituximab-induced apoptosis through miR-155-mediated Akt activation and up-regulation of Mcl-1. Leukemia & Lymphoma, 53(8), 1586–1591.CrossRef
104.
Zurück zum Zitat Pu, J., et al. (2012). Adrenaline promotes cell proliferation and increases chemoresistance in colon cancer HT29 cells through induction of miR-155. Biochemical and Biophysical Research Communications, 428(2), 210–215.PubMedCrossRef Pu, J., et al. (2012). Adrenaline promotes cell proliferation and increases chemoresistance in colon cancer HT29 cells through induction of miR-155. Biochemical and Biophysical Research Communications, 428(2), 210–215.PubMedCrossRef
105.
Zurück zum Zitat Bayraktar, R., Van Roosbroeck, K., & Calin, G. A. (2017). Cell-to-cell communication: microRNAs as hormones. Molecular Oncology, 11(12), 1673–1686.PubMedPubMedCentralCrossRef Bayraktar, R., Van Roosbroeck, K., & Calin, G. A. (2017). Cell-to-cell communication: microRNAs as hormones. Molecular Oncology, 11(12), 1673–1686.PubMedPubMedCentralCrossRef
106.
Zurück zum Zitat Chen, L., et al. (2014). miR-155 mediates drug resistance in osteosarcoma cells via inducing autophagy. Experimental and Therapeutic Medicine, 8(2), 527–532.PubMedPubMedCentralCrossRef Chen, L., et al. (2014). miR-155 mediates drug resistance in osteosarcoma cells via inducing autophagy. Experimental and Therapeutic Medicine, 8(2), 527–532.PubMedPubMedCentralCrossRef
107.
Zurück zum Zitat Patel, G. K., et al. (2017). Exosomes confer chemoresistance to pancreatic cancer cells by promoting ROS detoxification and miR-155-mediated suppression of key gemcitabine-metabolising enzyme, DCK. Br J Cancer, 116(5), 609–619.PubMedCrossRef Patel, G. K., et al. (2017). Exosomes confer chemoresistance to pancreatic cancer cells by promoting ROS detoxification and miR-155-mediated suppression of key gemcitabine-metabolising enzyme, DCK. Br J Cancer, 116(5), 609–619.PubMedCrossRef
108.
Zurück zum Zitat Mikamori, M., et al. (2017). MicroRNA-155 controls exosome synthesis and promotes gemcitabine resistance in pancreatic ductal adenocarcinoma. Scientific Reports, 7, 42339.PubMedPubMedCentralCrossRef Mikamori, M., et al. (2017). MicroRNA-155 controls exosome synthesis and promotes gemcitabine resistance in pancreatic ductal adenocarcinoma. Scientific Reports, 7, 42339.PubMedPubMedCentralCrossRef
109.
Zurück zum Zitat Lei, H., & Quelle, F. W. (2009). FOXO transcription factors enforce cell cycle checkpoints and promote survival of hematopoietic cells after DNA damage. Molecular Cancer Research, 7(8), 1294–1303.PubMedCrossRef Lei, H., & Quelle, F. W. (2009). FOXO transcription factors enforce cell cycle checkpoints and promote survival of hematopoietic cells after DNA damage. Molecular Cancer Research, 7(8), 1294–1303.PubMedCrossRef
110.
Zurück zum Zitat Lv, H., et al. (2014). miR-155 inhibitor reduces the proliferation and migration in osteosarcoma MG-63 cells. Experimental and Therapeutic Medicine, 8(5), 1575–1580.PubMedPubMedCentralCrossRef Lv, H., et al. (2014). miR-155 inhibitor reduces the proliferation and migration in osteosarcoma MG-63 cells. Experimental and Therapeutic Medicine, 8(5), 1575–1580.PubMedPubMedCentralCrossRef
111.
Zurück zum Zitat Feng, M., et al. (2015). Seed targeting with tiny anti-miR-155 inhibits malignant progression of multiple myeloma cells. Journal of Drug Targeting, 23(1), 59–66.PubMedCrossRef Feng, M., et al. (2015). Seed targeting with tiny anti-miR-155 inhibits malignant progression of multiple myeloma cells. Journal of Drug Targeting, 23(1), 59–66.PubMedCrossRef
112.
Zurück zum Zitat Meng, W., et al. (2012). Anti-miR-155 oligonucleotide enhances chemosensitivity of U251 cell to taxol by inducing apoptosis. Cell Biology International, 36(7), 653–659.PubMedCrossRef Meng, W., et al. (2012). Anti-miR-155 oligonucleotide enhances chemosensitivity of U251 cell to taxol by inducing apoptosis. Cell Biology International, 36(7), 653–659.PubMedCrossRef
113.
Zurück zum Zitat Choi, C. H., et al. (2012). Angiotensin II type I receptor and miR-155 in endometrial cancers: synergistic antiproliferative effects of anti-miR-155 and losartan on endometrial cancer cells. Gynecologic Oncology, 126(1), 124–131.PubMedCrossRef Choi, C. H., et al. (2012). Angiotensin II type I receptor and miR-155 in endometrial cancers: synergistic antiproliferative effects of anti-miR-155 and losartan on endometrial cancer cells. Gynecologic Oncology, 126(1), 124–131.PubMedCrossRef
114.
Zurück zum Zitat Zhang, M., et al. (2013). Lactosylated gramicidin-based lipid nanoparticles (Lac-GLN) for targeted delivery of anti-miR-155 to hepatocellular carcinoma. Journal of Controlled Release, 168(3), 251–261.PubMedPubMedCentralCrossRef Zhang, M., et al. (2013). Lactosylated gramicidin-based lipid nanoparticles (Lac-GLN) for targeted delivery of anti-miR-155 to hepatocellular carcinoma. Journal of Controlled Release, 168(3), 251–261.PubMedPubMedCentralCrossRef
115.
Zurück zum Zitat Mignacca, L., et al. (2016). Sponges against miR-19 and miR-155 reactivate the p53-Socs1 axis in hematopoietic cancers. Cytokine, 82, 80–86.PubMedCrossRef Mignacca, L., et al. (2016). Sponges against miR-19 and miR-155 reactivate the p53-Socs1 axis in hematopoietic cancers. Cytokine, 82, 80–86.PubMedCrossRef
116.
Zurück zum Zitat Khalife, J., et al. (2015). Pharmacological targeting of miR-155 via the NEDD8-activating enzyme inhibitor MLN4924 (Pevonedistat) in FLT3-ITD acute myeloid leukemia. Leukemia, 29(10), 1981–1992.PubMedPubMedCentralCrossRef Khalife, J., et al. (2015). Pharmacological targeting of miR-155 via the NEDD8-activating enzyme inhibitor MLN4924 (Pevonedistat) in FLT3-ITD acute myeloid leukemia. Leukemia, 29(10), 1981–1992.PubMedPubMedCentralCrossRef
117.
Zurück zum Zitat Querfeld, C., et al. (2016). Preliminary results of a phase II trial evaluating MRG-106, a synthetic microRNA antagonist (LNA antimiR) of microRNA-155, in patients with CTCL. Blood, 128(22), 1229. Querfeld, C., et al. (2016). Preliminary results of a phase II trial evaluating MRG-106, a synthetic microRNA antagonist (LNA antimiR) of microRNA-155, in patients with CTCL. Blood, 128(22), 1229.
118.
Zurück zum Zitat Catela Ivkovic, T., et al. (2017). microRNAs as cancer therapeutics: a step closer to clinical application. Cancer Letters, 407, 113–122.PubMedCrossRef Catela Ivkovic, T., et al. (2017). microRNAs as cancer therapeutics: a step closer to clinical application. Cancer Letters, 407, 113–122.PubMedCrossRef
Metadaten
Titel
miR-155 in cancer drug resistance and as target for miRNA-based therapeutics
verfasst von
Recep Bayraktar
Katrien Van Roosbroeck
Publikationsdatum
27.12.2017
Verlag
Springer US
Erschienen in
Cancer and Metastasis Reviews / Ausgabe 1/2018
Print ISSN: 0167-7659
Elektronische ISSN: 1573-7233
DOI
https://doi.org/10.1007/s10555-017-9724-7

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