Evaluation of the AntimiR-182 Effects on the Cisplatin Sensitivity in Hela Cells
DOI:
https://doi.org/10.22100/jkh.v10i4.844Keywords:
کلمات کلیدی, miRNA-182،antimiR-182،cell Hela ، CisplatinAbstract
Introduction: MicroRNAs (miRNAs) are single-stranded noncoding RNAs of 21–23 nucleotides that are not translated and have a basic role in gene expression.. They have an important role as a oncogene or tumor suppressor in human cancers.It has been reported that miR-182 in cervical cancer is an oncogene which is inhibited apoptosis in tumor cells. The aims of this study was evaluation of the miR-182 inhibition effect on induction of apoptosis in Cisplatin treated Hela cells.
Methods: The Hela cells were cultured and treated with different doses of Cisplatin, then viability of cells was assessed with MTT and LD50 of Cisplatin in hela cells obtained. The transfection condition was optimized by using serial dose of lipofectamine and labeled control miR, then optimum concentration of AntimiR-182 was calculated. Finally, AntimiR-182 and cisplatin separately and simultaneously were transfected into Hela cells, and the reduction in cell proliferation and increased of apoptosis rate of treated cells were analyzed by MTT and flow cytometric assay.
Results: The Hela cells which is transfected with both AntimiR-182 and cisplatin became more sensitive to cell death than cells which treated with cisplatin only. We found a significantly increase in cell death (apoptosis and necrosis) from 68% to 81% following the transfection with AntimiR-182 and cisplatin (P<0.05).
Conclusion: The results of the present study shows that expression of miR-182 may have a significant effect in resistance of tumor cells to chemotherapy. Using simultaneously of AntimiR-182 and cisplatin have an additional effect on cisplatin, so, it reduces LD50 of cisplatin. Therefore, AntimiR-182 can be used as a complementary methods of treatment for increasing sensitivity of tumor cells to treatment and decreasing drug resistance.
References
منابع
Guillermo TL, Eduardol F. Epidemiology of cervical vulvar and vaginal cancer. In: Gershenson DM, Guire WP, Gore M, Quinn MA, Thomas G. Gynecologic cancer controversies in management. Philadelphia:Elsveir;2004:p.913.
Pisani, P., The cancer burden and cancer control in developing countries. Environmental Health, 2011. 10(Suppl 1): p. S2.
Boring CC, Squiers TS, Tong T. Cancer Statics, 1994. CA Cancer Clin 1993; 44:7-26.
H.W. Hwang, J.T. Mendel. MicroRNAs in cell proliferation, cell death, and tumorigenesis. Br. J. Cancer, 94 (2006), pp. 776–780
B. Bao, S. Ali, D. Kong, et al. Anti-tumor activity of a novel compound-CDF is mediated by regulating miR-21, miR-200, and PTEN in pancreatic cancer . PLoS One, 6 (2011), p. e17850
Y. Saito, H. Suzuki, H. Tsugawa, et al. Chromatin remodeling at Alu repeats by epigenetic treatment activates silenced microRNA-512-5p with downregulation of Mcl-1 in human gastric cancer cells. Oncogene, 28 (2009), pp. 2738–2744
Wang Z, Luo X, Lu Y, Yang B. miRNAs at the heart of the matter. J Mol Med 2008; 86: 771-83.
Garzon R, Fabbri M, Cimmino A, Calin GA, Croce CM MicroRNA expression and function in cancer. Trends Mol Med.2006. 12: 580–58
Q. Xie, X. Chen, F. Lu, et al. Aberrant expression of microRNA 155 may accelerate cell proliferation by targeting sex-determining region Y box 6 in hepatocellular carcinoma. Cancer, 2012: 118, pp. 2431–2442
Y. Zhang, W. Wei, N. Cheng, et al Hepatitis C virus-induced up-regulation of microRNA-155 promotes hepatocarcinogenesis by activating Wnt signaling. Hepatology, 2012: 56, pp. 1631–1640
Y. Tomimaru, H. Eguchi, H. Nagano, et al. MicroRNA-21 induces resistance to the anti-tumour effect of interferon-alpha/5-fluorouracil in hepatocellular carcinoma cells. Br. J. Cancer, 2010: 103, pp. 1617–1626
T.P. Robin, A. Smith, E. McKinsey, L. Reaves, P. Jedlicka, H.L. Ford. EWS/FLI1 regulates EYA3 in Ewing sarcoma via modulation of miRNA-708, resulting in increased cell survival and chemoresistance. Mol. Cancer Res., 2012: 10, pp. 1098–1108
Elmen, J., et al., LNA-mediated microRNA silencing in non-human primates. Nature, 2008. 452(7189): p. 896-9
R. Lei, J. Tang, X. Zhuang, et al. Suppression of MIM by microRNA-182 activates RhoA and promotes breast cancer metastasis. Oncogene (2013) http://dx.doi.org/10.1038/onc.2013.65
H. Wang, G. Tan, L. Dong, et al. Circulating MiR-125b as a marker predicting chemoresistance in breast cancer. PLoS One, 2012: 7, p. e34210
Y.Q. Wang, R.D. Guo, R.M. Guo, W. Sheng, L.R. Yin MicroRNA-182 promotes cell growth, invasion, and chemoresistance by targeting programmed cell death 4 (PDCD4) in human ovarian carcinomas. J. Cell. Biochem., 2013: 114, pp. 1464–1473
S. Husted, R. Sokilde, L. Rask, et al. MicroRNA expression profiles associated with development of drug resistance in Ehrlich ascites tumor cells Mol. Pharm., 2011: 8, pp. 2055–2062
Tang, T., et al., MicroRNA-182 plays an onco-miRNA role in cervical cancer. Gynecol Oncol, 2013. 129(1): p. 199-208.
Gong, C., et al., Up-regulation of miR-21 mediates resistance to trastuzumab therapy for breast cancer. J Biol Chem, 2011. 286(21): p. 19127-37.
Lagos-Quintana M, Rauhut R, Lendeckel W, Tuschl T Identification of novel genes coding for small expressed RNAs. Science . 2001,294: 853–858
Ambros V. The functions of animal microRNAs. Nature 2004;431:350e355.
Bartel DP. Multiple miRNAs participated in tumorigenesis and development. Cell 2004;116:281e297.
Rajewsky N, Socci ND Computational identification of microRNA targets. Dev Biol. 2004, 267: 529–535
Chen X A microRNA as a translational repressor of APETALA2 in Arabidopsis flower development. Science.2004. 303: 2022–2025
Poy MN, Eliasson L, Krutzfeldt J, Kuwajima S, Ma X, et al. A pancreatic islet-specific microRNA regulates insulin secretion. Nature. 2004. 432: 226–230
Munker R, Calin GA. MicroRNA profiling in cancer. Clin Sci (Lond) 2011;121: 141–58.
Esquela-Kerscher A, Slack FJ. Oncomirs — microRNAs with a role in cancer. Nat Rev Cancer 2006;6:259–69.
Hirata H, Ueno K, Shahryari V, Deng G, Tanaka Y, Tabatabai ZL, Hinoda Y, Dahiya R: MicroRNA-182-5p promotes cell invasion and proliferation by down regulating FOXF2, RECK and MTSS1 genes in human prostate cancer. PLoS One 2013, 8:e55502
Chiang CH, Hou MF, Hung WC: Up-regulation of miR-182 by beta-catenin in breast cancer increases tumorigenicity and invasiveness by targeting the matrix metalloproteinase inhibitor RECK. Biochim Biophys Acta 1830 2013:3067–3076.
Lui WO, Pourmand N, Patterson BK, Fire A. Patterns of known and novel small RNAs in human cervical cancer. Cancer Res 2007;67:6031–43.
Wang X, Tang S, Le SY, Lu R, Rader JS, Meyers C, et al. Aberrant expression of oncogenic and tumor-suppressive microRNAs in cervical cancer is required for
Cancer cell growth. PLoS One 2008;3:e2557.
Tao J, Lu Q, Wu D, et al. microRNA-21 modulates cell proliferation and sensitivity to doxorubicin in bladder cancer cells. Oncol Rep 2011;25:1721e1729
Ning, F.L., et al., MicroRNA-182 modulates chemosensitivity of human non-small cell lung cancer to cisplatin by targeting PDCD4. Diagn Pathol, 2014. 9: p. 143.
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