Effects of miR-200c on the migration and invasion abilities of human prostate cancer Du145 cells and the corresponding mechanism
Runlin Shi, Haibing Xiao, Tao Yang, Lei Chang, Yuanfeng Tian, Bolin Wu, Hua Xu
Effects of miR-200c on the migration and invasion abilities of human prostate cancer Du145 cells and the corresponding mechanism
microRNAs (miRNAs) have played a key role in human tumorigenesis, tumor progression, and metastasis. On the one hand, miRNAs are aberrantly expressed in many types of human cancer; on the other hand, miRNAs can function as tumor suppressors or oncogenes that target many cancer-related genes. This study aimed to investigate the effects of miRNA-200c (miR-200c) on the biological behavior and mechanism of proliferation, migration, and invasion in the prostate cancer cell line Du145. In this study, Du145 cells were transfected with miR-200c mimics or negative control miR-NC by using an X-tremeGENE siRNA transfection reagent. The relative expression of miR-200c was measured by RT-PCR. The proliferation, migration, and invasion abilities of Du145 cells were detected by CCK8 assays, migration assays and invasion assays, respectively. The expressions of ZEB1, E-cadherin, and vimentin were observed by western blot. Results showed that DU145 cells exhibited a high expression of miR-200c compared with immortalized normal prostate epithelial cell RWPE-1. Du145 cells were then transfected with miR-200c mimics and displayed lower abilities of proliferation, migration, and invasion than those transfected with the negative control. The protein levels of ZEB1 and vimentin were expressed at a low extent in Du145 cells, which were transfected with miR-200c mimics; by contrast, E-cadherin was highly expressed. Hence, miR-200c could significantly inhibit the proliferation of the prostate cancer cell line Du145; likewise, miR-200c could inhibit migration and invasion by epithelial-mesenchymal transition.
miR-200c / proliferation / migration / invasion / prostate cancer / Du145 cell / ZEB1
[1] |
Zhu X, Gerstein M, Snyder M. Getting connected: analysis and principles of biological networks. Genes Dev2007; 21(9): 1010-1024
CrossRef
Pubmed
Google scholar
|
[2] |
Ruvkun G. Molecular biology. Glimpses of a tiny RNA world. Science2001; 294(5543): 797-799
CrossRef
Pubmed
Google scholar
|
[3] |
Ambs S, Prueitt RL, Yi M, Hudson RS, Howe TM, Petrocca F, Wallace TA, Liu CG, Volinia S, Calin GA, Yfantis HG, Stephens RM, Croce CM. Genomic profiling of microRNA and messenger RNA reveals deregulated microRNA expression in prostate cancer. Cancer Res2008; 68(15): 6162-6170
CrossRef
Pubmed
Google scholar
|
[4] |
Dalmay T, Edwards DR. MicroRNAs and the hallmarks of cancer. Oncogene2006; 25(46): 6170-6175
CrossRef
Pubmed
Google scholar
|
[5] |
Brabletz S, Brabletz T. The ZEB/miR-200 feedback loop—a motor of cellular plasticity in development and cancer? EMBO Rep2010; 11(9): 670-677
CrossRef
Pubmed
Google scholar
|
[6] |
Cochrane DR, Spoelstra NS, Howe EN, Nordeen SK, Richer JK. MicroRNA-200c mitigates invasiveness and restores sensitivity to microtubule-targeting chemotherapeutic agents. Mol Cancer Ther2009; 8(5): 1055-1066
CrossRef
Pubmed
Google scholar
|
[7] |
Cochrane DR, Howe EN, Spoelstra NS, Richer JK. Loss of miR-200c: a marker of aggressiveness and chemoresistance in female reproductive cancers. J Oncol2010; 2010: 821717
CrossRef
Pubmed
Google scholar
|
[8] |
Cittelly DM, Dimitrova I, Howe EN, Cochrane DR, Jean A, Spoelstra NS, Post MD, Lu X, Broaddus RR, Spillman MA, Richer JK. Restoration of miR-200c to ovarian cancer reduces tumor burden and increases sensitivity to paclitaxel. Mol Cancer Ther2012; 11(12): 2556-2565
CrossRef
Pubmed
Google scholar
|
[9] |
Thiery JP. Epithelial-mesenchymal transitions in tumour progression. Nat Rev Cancer2002; 2(6): 442-454
CrossRef
Pubmed
Google scholar
|
[10] |
Yang J, Weinberg RA. Epithelial-mesenchymal transition: at the crossroads of development and tumor metastasis. Dev Cell2008; 14(6): 818-829
CrossRef
Pubmed
Google scholar
|
[11] |
Acloque H, Adams MS, Fishwick K, Bronner-Fraser M, Nieto MA. Epithelial-mesenchymal transitions: the importance of changing cell state in development and disease. J Clin Invest2009; 119(6): 1438-1449
CrossRef
Pubmed
Google scholar
|
[12] |
Kalluri R, Weinberg RA. The basics of epithelial-mesenchymal transition. J Clin Invest2009; 119(6): 1420-1428
CrossRef
Pubmed
Google scholar
|
[13] |
Polyak K, Weinberg RA. Transitions between epithelial and mesenchymal states: acquisition of malignant and stem cell traits. Nat Rev Cancer2009; 9(4): 265-273
CrossRef
Pubmed
Google scholar
|
[14] |
Thiery JP, Acloque H, Huang RY, Nieto MA. Epithelial-mesenchymal transitions in development and disease. Cell2009; 139(5): 871-890
CrossRef
Pubmed
Google scholar
|
[15] |
Chen Y, Sun Y, Chen L, Xu X, Zhang X, Wang B, Min L, Liu W. miRNA-200c increases the sensitivity of breast cancer cells to doxorubicin through the suppression of E-cadherin-mediated PTEN/Akt signaling. Mol Med Rep2013; 7(5): 1579-1584
Pubmed
|
[16] |
Hurteau GJ, Carlson JA, Spivack SD, Brock GJ. Overexpression of the microRNA hsa-miR-200c leads to reduced expression of transcription factor 8 and increased expression of E-cadherin. Cancer Res2007; 67(17): 7972-7976
CrossRef
Pubmed
Google scholar
|
[17] |
Wang J, Ruan K. miR-200c affects the mRNA expression of E-cadherin by regulating the mRNA level of TCF8 during post-natal epididymal development in juvenile rats. Acta Biochim Biophys Sin (Shanghai)2010; 42(9): 628-634
CrossRef
Pubmed
Google scholar
|
[18] |
Chen ML, Liang LS, Wang XK. miR-200c inhibits invasion and migration in human colon cancer cells SW480/620 by targeting ZEB1. Clin Exp Metastasis2012; 29(5): 457-469
CrossRef
Pubmed
Google scholar
|
[19] |
Burk U, Schubert J, Wellner U, Schmalhofer O, Vincan E, Spaderna S, Brabletz T. A reciprocal repression between ZEB1 and members of the miR-200 family promotes EMT and invasion in cancer cells. EMBO Rep2008; 9(6): 582-589
CrossRef
Pubmed
Google scholar
|
[20] |
Zhang H, Li Y, Lai M. The microRNA network and tumor metastasis. Oncogene2010; 29(7): 937-948
CrossRef
Pubmed
Google scholar
|
[21] |
Ocaña OH, Nieto MA. A new regulatory loop in cancer-cell invasion. EMBO Rep2008; 9(6): 521-522
CrossRef
Pubmed
Google scholar
|
[22] |
Lin J, Liu C, Gao F, Mitchel RE, Zhao L, Yang Y, Lei J, Cai J. miR-200c enhances radiosensitivity of human breast cancer cells. J Cell Biochem2013; 114(3): 606-615
CrossRef
Pubmed
Google scholar
|
[23] |
Voorhoeve PM. MicroRNAs: Oncogenes, tumor suppressors or master regμlators of cancer heterogeneity? Biochimica et biophysica acta2010; 1805: 72-86.
|
[24] |
Chuang TD, Panda H, Luo X, Chegini N. miR-200c is aberrantly expressed in leiomyomas in an ethnic-dependent manner and targets ZEBs, VEGFA, TIMP2, and FBLN5. Endocr Relat Cancer2012; 19(4): 541-556
CrossRef
Pubmed
Google scholar
|
[25] |
Park YA, Lee JW, Choi JJ, Jeon HK, Cho Y, Choi C, Kim TJ, Lee NW, Kim BG, Bae DS. The interactions between MicroRNA-200c and BRD7 in endometrial carcinoma. Gynecol Oncol2012; 124(1): 125-133
CrossRef
Pubmed
Google scholar
|
[26] |
Hamano R, Miyata H, Yamasaki M, Kurokawa Y, Hara J, Moon JH, Nakajima K, Takiguchi S, Fujiwara Y, Mori M, Doki Y. Overexpression of miR-200c induces chemoresistance in esophageal cancers mediated through activation of the Akt signaling pathway. Clin Cancer <?Pub Caret?>Res2011; 17: 3029-3038
|
[27] |
Adam L, Zhong M, Choi W, Qi W, Nicoloso M, Arora A, Calin G, Wang H, Siefker-Radtke A, McConkey D, Bar-Eli M, Dinney C. miR-200 expression regμlates epithelial-to-mesenchymal transition in bladder cancer cells and reverses resistance to epidermal growth factor receptor therapy. Clin Cancer Res2009; 15: 5060-5072
|
[28] |
Jurmeister S, Baumann M, Balwierz A, Keklikoglou I, Ward A, Uhlmann S, Zhang JD, Wiemann S, Sahin O. MicroRNA-200c represses migration and invasion of breast cancer cells by targeting actin-regμlatory proteins FHOD1 and PPM1F. Mol Cell Biol2012; 32: 633-651
|
[29] |
Banyard J, Chung I, Wilson AM, Vetter G, Le Béchec A, Bielenberg DR, Zetter BR. Regulation of epithelial plasticity by miR-424 and miR-200 in a new prostate cancer metastasis model. Sci Rep2013; 3: 3151
CrossRef
Pubmed
Google scholar
|
[30] |
Kim J, Wu L, Zhao JC, Jin HJ, Yu J. TMPRSS2-ERG gene fusions induce prostate tumorigenesis by modulating microRNA miR-200c. Oncogene2013<month>Nov</month><day>4</day>. [Epub ahead of print]
CrossRef
Pubmed
Google scholar
|
[31] |
Hurteau GJ, Carlson JA, Spivack SD, Brock GJ. Overexpression of the microRNA hsa-miR-200c leads to reduced expression of transcription factor 8 and increased expression of E-cadherin. Cancer Res2007; 67(17): 7972-7976
CrossRef
Pubmed
Google scholar
|
[32] |
Kong D, Li Y, Wang Z, Banerjee S, Ahmad A, Kim HR, Sarkar FH. miR-200 regulates PDGF-D-mediated epithelial-mesenchymal transition, adhesion, and invasion of prostate cancer cells. Stem Cells2009; 27(8): 1712-1721
CrossRef
Pubmed
Google scholar
|
[33] |
Murray D, Precht P, Balakir R, Horton WE Jr. The transcription factor deltaEF1 is inversely expressed with type II collagen mRNA and can repress Col2a1 promoter activity in transfected chondrocytes. J Biol Chem2000; 275(5): 3610-3618
CrossRef
Pubmed
Google scholar
|
[34] |
Song Y, Zhang Y, Wu H, Kong M, Chen X, Shao C. The relationships between zeb1 and the migration ability of tumor cells. World Chin J Digestology (Shi Jie Hua Ren Xiao Hua Za Zhi)2010; 18(11): 1099-1103 (in chinese)
|
[35] |
Gregory PA, Bert AG, Paterson EL, Barry SC, Tsykin A, Farshid G, Vadas MA, Khew-Goodall Y, Goodall GJ. The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1. Nat Cell Biol2008; 10(5): 593-601
CrossRef
Pubmed
Google scholar
|
[36] |
Hurteau GJ, Carlson JA, Roos E, Brock GJ. Stable expression of miR-200c alone is sufficient to regulate TCF8 (ZEB1) and restore E-cadherin expression. Cell Cycle2009; 8(13): 2064-2069
CrossRef
Pubmed
Google scholar
|
[37] |
Liu C, Kelnar K, Liu B, Chen X, Calhoun-Davis T, Li H, Patrawala L, Yan H, Jeter C, Honorio S, Wiggins JF, Bader AG, Fagin R, Brown D, Tang DG. The microRNA miR-34a inhibits prostate cancer stem cells and metastasis by directly repressing CD44. Nat Med2011; 17(2): 211-215
CrossRef
Pubmed
Google scholar
|
/
〈 | 〉 |