Effect of miR-892a on the proliferation and migration of prostate cancer cells by targeting SOX5
Han Bing1, Mao Likai2, Guan Han1, Zhang Chong1, Yao Yue1, Xiong Yanjun1, Gao Xingfu1, Wang Sheng1
1Department of Urology, the First Affiliated Hospital of Bengbu Medical College, Bengbu 233004, China; 2Department of Urology, the Second Affiliated Hospital of Bengbu Medical College, Bengbu 233040, China
Abstract：Objective To explore the effect of miR-892a on the proliferation and migration of prostate cancer cells.Methods The miRNA expression data of prostate cancer and adjacent tissues were downloaded from The Cancer Genome Atlas datasets. Limma and Gplots of RStudio software were used in differential expression analysis to draw volcanic and heat maps. MiR-892a expression in prostate epithelial cells (RWPE-1) and prostate cancer cells (DU145 and PC3) was detected by reverse-transcription polymerase chain reaction (RT-PCR). In vitro cell proliferation was measured by methyl thiazolyl tetrazolium(MTT) assay. Low-density cell colony formation experiment was performed after transforming with miR-892a mimic or negative control (NC). Transwell migration experiment was carried out to investigate cell migration ability. MiRNA prediction website was used to predict the potential target of miR-892a. The binding of miR-892a to SOX5 was verified by western blot,RT-PCR and dual-luciferase reporter gene experiment.Results MiR-892a was chose as the target gene. MiR-892a expression was lower in prostate cancer cells than in RWPE-1 cells (PC3, 0.41±0.40; DU145, 0.47±0.45; RWPE, 1.18±0.35; P＜0.05); thus, PC3 was used as the subsequent research subject. Compared with miR-NC, miR-892a mimic could decrease cell proliferation ability as determined by MTT assay (P＜0.05), and low-density cell colony formation experiment (NC, 433.28±62.93; mimic, 251.00±64.84; P＜0.05), and could decrease migration ability as determined by transwell migration experiment (NC, 534.33±61.07; miR-892a mimic, 340.33±31.30; P＜0.05). SOX5 protein expression was found lower in the cells with miR-892a mimic than those with miR-NC (NC, 0.519±0.014; miR-892a mimic, 0.196±0.019; P＜0.01), and the mRNA of SOX5 had a similar result (NC, 1.021±0.012; miR-892a mimic, 0.156±0.017; P＜0.01). MiR-892a was capable of binding to the 3' untranslated region of SOX5 directly as determined by dual-luciferase reporter gene experiment (NC,0.97±0.10; miR-892a mimic, 0.37±0.08; P＜0.01).Conclusions Comparing with in prostate epithelial cells, miR-892a is down-regulated in prostate cancer cells. miR-892a overexpression can inhibit the proliferation and migration of prostate cancer cells by targeting SOX5.
韩兵, 毛溧凯, 关翰, 张冲, 姚越, 熊言骏, 高幸福, 汪盛. miR-892a靶向调控SOX5对前列腺癌细胞增殖和迁移能力的影响[J]. 中华解剖与临床杂志, 2021, 26(3): 346-351.
Han Bing, Mao Likai, Guan Han, Zhang Chong, Yao Yue, Xiong Yanjun, Gao Xingfu, Wang Sheng. Effect of miR-892a on the proliferation and migration of prostate cancer cells by targeting SOX5. Chinese Journal of Anatomy and Clinics, 2021, 26(3): 346-351.
Catalona WJ, Richie JP, Ahmann FR, et al. Comparison of digital rectal examination and serum prostate specific antigen in the early detection of prostate cancer: results of a multicenter clinical trial of 6, 630 men[J]. J Urol, 2017, 197(2S): S200-S207. DOI:10.1016/j.juro.2016.10.073.
[2]
Bill-Axelson A, Holmberg L, Ruutu M, et al. Radical prostatectomy versus watchful waiting in early prostate cancer[J]. N Engl J Med, 2011, 364(18): 1708-1717. DOI:10.1056/NEJMoa1011967.
[3]
Joniau S, Briganti A, Gontero P, et al. Stratification of high-risk prostate cancer into prognostic categories: a European multi-institutional study[J]. Eur Urol, 2015, 67(1): 157-164. DOI:10.1016/j.eururo.2014.01.020.
[4]
Pritchard CC, Cheng HH, Tewari M. MicroRNA profiling: approaches and considerations[J]. Nat Rev Genet, 2012, 13(5): 358-369. DOI:10.1038/nrg3198.
[5]
Bai P, Li W, Wan Z, et al. MiR-489-3p Inhibits prostate cancer progression by targeting DLX1[J]. Cancer Manag Res, 2020, 12: 2719-2729. DOI:10.2147/CMAR.S239796.
[6]
Zhao Z, Zhao S, Luo L, et al. MiR-199b-5p-DDR1-ERK signalling axis suppresses prostate cancer metastasis via inhibiting epithelial-mesenchymal transition[J]. Br J Cancer, 2021, 124(5): 982-994. DOI:10.1038/s41416-020-01187-8.
[7]
Lv J, Zhang H, Gao Z, et al. Prognostic value of miR-892a in gastric cancer and its regulatory effect on tumor progression[J]. Cancer Biomark, 2020, 28(2): 247-254. DOI:10.3233/CBM-191323.
[8]
Jia B, Tan L, Jin Z, et al. MiR-892a promotes hepatocellular carcinoma cells proliferation and invasion through targeting CD226[J]. J Cell Biochem, 2017, 118(6): 1489-1496. DOI:10.1002/jcb.25808.
[9]
Liang WL, Cao J, Xu B, et al. MiR-892a regulated PPP2R2A expression and promoted cell proliferation of human colorectal cancer cells[J]. Biomed Pharmacother, 2015, 72: 119-124. DOI:10.1016/j.biopha.2015.04.015.
[10]
Fendler A, Jung M, Stephan C, et al. MiRNAs can predict prostate cancer biochemical relapse and are involved in tumor progression[J]. Int J Oncol, 2011, 39(5): 1183-1192. DOI:10.3892/ijo.2011.1128.
[11]
Malik SS, Batool R, Masood N, et al. Risk factors for prostate cancer: a multifactorial case-control study[J]. Curr Probl Cancer, 2018, 42(3): 337-343. DOI:10.1016/j.currproblcancer.2018.01.014.
[12]
Filipowicz W, Bhattacharyya SN, Sonenberg N. Mechanisms of post-transcriptional regulation by microRNAs: are the answers in sight?[J]. Nat Rev Genet, 2008, 9(2): 102-114. DOI:10.1038/nrg2290.
[13]
Friedman RC, Farh KK, Burge CB, et al. Most mammalian mRNAs are conserved targets of microRNAs[J]. Genome Res, 2009, 19(1): 92-105. DOI:10.1101/gr.082701.108.
[14]
Iorio MV, Croce CM. MicroRNA involvement in human cancer[J]. Carcinogenesis, 2012, 33(6): 1126-1133. DOI:10.1093/carcin/bgs140.
[15]
Hanahan D, Weinberg RA. Hallmarks of cancer: the next generation[J]. Cell, 2011, 144(5): 646-674. DOI:10.1016/j.cell.2011.02.013.
[16]
Hainaut P, Plymoth A. Targeting the hallmarks of cancer: towards a rational approach to next-generation cancer therapy[J]. Curr Opin Oncol, 2013, 25(1): 50-51. DOI:10.1097/CCO.0b013e32835b651e.
[17]
Baroti T, Zimmermann Y, Schillinger A, et al. Transcription factors Sox5 and Sox6 exert direct and indirect influences on oligodendroglial migration in spinal cord and forebrain[J]. Glia, 2016, 64(1): 122-138. DOI:10.1002/glia.22919.
[18]
Renjie W, Haiqian L. MiR-132, miR-15a and miR-16 synergistically inhibit pituitary tumor cell proliferation, invasion and migration by targeting Sox5[J]. Cancer Lett, 2015, 356(2 Pt B): 568-578. DOI:10.1016/j.canlet.2014.10.003.
[19]
Sun C, Ban Y, Wang K, et al. SOX5 promotes breast cancer proliferation and invasion by transactivation of EZH2[J]. Oncol Lett, 2019, 17(3): 2754-2762. DOI:10.3892/ol.2019.9914.
[20]
Wang D, Han S, Wang X, et al. SOX5 promotes epithelial-mesenchymal transition and cell invasion via regulation of Twist1 in hepatocellular carcinoma[J]. Med Oncol, 2015, 32(2): 461. DOI:10.1007/s12032-014-0461-2.
[21]
Zou H, Wang S, Wang S, et al. SOX5 interacts with YAP1 to drive malignant potential of non-small cell lung cancer cells[J]. Am J Cancer Res, 2018, 8(5): 866-878.
[22]
Xu J, Kang Y, Liao WM, et al. MiR-194 regulates chondrogenic differentiation of human adipose-derived stem cells by targeting Sox5[J]. PLoS One, 2012, 7(3): e31861. DOI:10.1371/journal.pone.0031861.
[23]
Wang P, Zhao Y, Fan R, et al. MicroRNA-21a-5p Functions on the regulation of melanogenesis by targeting Sox5 in mouse skin melanocytes[J]. Int J Mol Sci, 2016, 17(7): 959. DOI:10.3390/ijms17070959.
[24]
Hu J, Tian J, Zhu S, et al. Sox5 contributes to prostate cancer metastasis and is a master regulator of TGF-β-induced epithelial mesenchymal transition through controlling Twist1 expression[J]. Br J Cancer, 2018, 118(1): 88-97. DOI:10.1038/bjc.2017.372.
[25]
Ma S, Chan YP, Woolcock B, et al. DNA fingerprinting tags novel altered chromosomal regions and identifies the involvement of SOX5 in the progression of prostate cancer[J]. Int J Cancer, 2009, 124(10): 2323-2332. DOI:10.1002/ijc.24243.
[26]
Yang B, Zhang W, Sun D, et al. Downregulation of miR-139-5p promotes prostate cancer progression through regulation of SOX5[J]. Biomed Pharmacother, 2019, 109: 2128-2135. DOI:10.1016/j.biopha.2018.09.029.
2021, Vol. 26 
