Comprehensive Study of Gene and microRNA Expression Related to Epithelial-Mesenchymal Transition in Prostate Cancer
Carregando...
Citações na Scopus
38
Tipo de produção
article
Data de publicação
2014
Título da Revista
ISSN da Revista
Título do Volume
Editora
PUBLIC LIBRARY SCIENCE
Citação
PLOS ONE, v.9, n.11, article ID e113700, 10p, 2014
Resumo
Prostate cancer is the most common cancer in men, and most patients have localized disease at the time of diagnosis. However, 4% already present with metastatic disease. Epithelial-mesenchymal transition is a fundamental process in carcinogenesis that has been shown to be involved in prostate cancer progression. The main event in epithelial-mesenchymal transition is the repression of E-cadherin by transcription factors, but the process is also regulated by microRNAs. The aim of this study was to analyze gene and microRNA expression involved in epithelial-mesenchymal transition in localized prostate cancer and metastatic prostate cancer cell lines and correlate with clinicopathological findings. We studied 51 fresh frozen tissue samples from patients with localized prostate cancer (PCa) treated by radical prostatectomy and three metastatic prostate cancer cell lines (LNCaP, DU145, PC3). The expression of 10 genes and 18 miRNAs were assessed by real-time PCR. The patients were divided into groups according to Gleason score, pathological stage, preoperative PSA, biochemical recurrence, and risk group for correlation with clinicopathological findings. The majority of localized PCa cases showed an epithelial phenotype, with overexpression of E-cadherin and underexpression of the mesenchymal markers. MiRNA-200 family members and miRNAs 203, 205, 183, 373, and 21 were overexpressed, while miRNAs 9, 495, 29b, and 1 were underexpressed. Low-expression levels of miRNAs 200b, 30a, and 1 were significantly associated with pathological stage. Lower expression of miR-200b was also associated with a Gleason score >= 8 and shorter biochemical recurrence-free survival. Furthermore, low-expression levels of miR-30a and high-expression levels of Vimentin and Twist1 were observed in the high-risk group. Compared with the primary tumor, the metastatic cell lines showed significantly higher expression levels of miR-183 and Twist1. In summary, miRNAs 200b, 30a, 1, and 183 and the genes Twist1 and Vimentin might play important roles in the progression of prostate cancer and may eventually become important prognostic markers.
Palavras-chave
Referências
- Ambs S, 2008, CANCER RES, V68, P6162, DOI 10.1158/0008-5472.CAN-08-0144
- Barron N, 2012, PROSTATE, V72, P1193, DOI 10.1002/pros.22469
- Bartel DP, 2004, CELL, V116, P281, DOI 10.1016/S0092-8674(04)00045-5
- Batlle E, 2000, NAT CELL BIOL, V2, P84, DOI 10.1038/35000034
- Behnsawy HM, 2013, BJU INT, V111, P30, DOI 10.1111/j.1464-410X.2012.11551.x
- Bendoraite A, 2010, GYNECOL ONCOL, V116, P117, DOI 10.1016/j.ygyno.2009.08.009
- Bethel CR, 2006, CANCER RES, V66, P10683, DOI 10.1158/0008-5472.CAN-06-0963
- Bracken CP, 2008, CANCER RES, V68, P7846, DOI 10.1158/0008-5472.CAN-08-1942
- Burk U, 2008, EMBO REP, V9, P582, DOI 10.1038/embor.2008.74
- Carlsson J, 2011, CANCER CELL INT, V11, DOI 10.1186/1475-2867-11-14
- Casas E, 2011, CANCER RES, V71, P245, DOI 10.1158/0008-5472.CAN-10-2330
- Cheng CW, 2012, BREAST CANCER RES TR, V134, P1081, DOI 10.1007/s10549-012-2034-4
- Ding ZH, 2011, NATURE, V470, P269, DOI 10.1038/nature09677
- Eide T, 2013, CANCER CELL INT, V13, DOI 10.1186/1475-2867-13-4
- Epstein JI, 2005, AM J SURG PATHOL, V29, P1228, DOI 10.1097/01.pas.0000173646.99337.b1
- Graham TR, 2008, CANCER RES, V68, P2479, DOI 10.1158/0008-5472.CAN-07-2559
- Gregory PA, 2008, NAT CELL BIOL, V10, P593, DOI 10.1038/ncb1722
- Halbleib JM, 2006, GENE DEV, V20, P3199, DOI 10.1101/gad.1486806
- Hu XX, 2009, GYNECOL ONCOL, V114, P457, DOI 10.1016/j.ygyno.2009.05.022
- Huber MA, 2005, CURR OPIN CELL BIOL, V17, P548, DOI 10.1016/j.ceb.2005.08.001
- Hudson RS, 2012, NUCLEIC ACIDS RES, V40, P3689, DOI 10.1093/nar/gkr1222
- Iwata T, 2010, PLOS ONE, V5, DOI 10.1371/journal.pone.0009427
- Kao CJ, 2013, ONCOGENE
- Kojima S, 2012, BRIT J CANCER, V106, P405, DOI 10.1038/bjc.2011.462
- Kong DJ, 2009, STEM CELLS, V27, P1712, DOI 10.1002/stem.101
- Korpal M, 2008, J BIOL CHEM, V283, P14910, DOI 10.1074/jbc.C800074200
- Kumarswamy R, 2012, INT J CANCER, V130, P2044, DOI 10.1002/ijc.26218
- Kurashige J, 2012, ANN SURG ONCOL, V19, pS656, DOI 10.1245/s10434-012-2217-6
- Kwok WK, 2005, CANCER RES, V65, P5153, DOI 10.1158/0008-5472.CAN-04-3785
- Li XL, 2014, MOL CELL BIOL, V34, P533, DOI 10.1128/MCB.01043-13
- Liu Y, 2012, MED SCI MONITOR, V18, pBR299
- Liu YN, 2008, MOL CELL BIOL, V28, P7096, DOI 10.1128/MCB.00449-08
- Liu YN, 2013, ONCOGENE, V32, P296, DOI 10.1038/onc.2012.58
- Ma L, 2007, NATURE, V449, P682, DOI 10.1038/nature06174
- Mackinnon AC, 2009, ARCH PATHOL LAB MED, V133, P1033, DOI 10.1043/1543-2165-133.7.1033
- Marchini S, 2011, LANCET ONCOL, V12, P273, DOI 10.1016/S1470-2045(11)70012-2
- Moreno-Bueno G, 2006, CANCER RES, V66, P9543, DOI 10.1158/0008-5472.CAN-06-0479
- Nam EJ, 2008, CLIN CANCER RES, V14, P2690, DOI 10.1158/1078-0432.CCR-07-1731
- Park SM, 2008, GENE DEV, V22, P894, DOI 10.1101/gad.1640608
- Paterson EL, 2008, THESCIENTIFICWORLDJO, V8, P901, DOI 10.1100/tsw.2008.115
- Porkka KP, 2007, CANCER RES, V67, P6130, DOI 10.1158/0008-5472.CAN-07-0533
- Putzke AP, 2011, AM J PATHOL, V179, P400, DOI 10.1016/j.ajpath.2011.03.028
- Qu Y, 2013, INT J CANCER, V133, P544, DOI 10.1002/ijc.28056
- Quinn DI, 2001, J CLIN ONCOL, V19, P3692
- Ru P, 2012, MOL CANCER THER, V11, P1166, DOI 10.1158/1535-7163.MCT-12-0100
- Sarver AL, 2010, CANCER RES, V70, P9570, DOI 10.1158/0008-5472.CAN-10-2074
- Siegel R, 2013, CA-CANCER J CLIN, V63, P11, DOI 10.3322/caac.21166
- Siemens H, 2011, CELL CYCLE, V10, P4256, DOI 10.4161/cc.10.24.18552
- Sun YT, 2012, CANCER RES, V72, P527, DOI 10.1158/0008-5472.CAN-11-3004
- Taylor BS, 2010, CANCER CELL, V18, P11, DOI 10.1016/j.ccr.2010.05.026
- Thiery JP, 2009, CELL, V139, P871, DOI 10.1016/j.cell.2009.11.007
- Tomita K, 2000, CANCER RES, V60, P3650
- Ueno K, 2013, BRIT J CANCER, V108, P1659, DOI 10.1038/bjc.2013.125
- Vernon AE, 2004, CURR BIOL, V14, pR719, DOI 10.1016/j.cub.2004.08.048
- Wang W, 2013, EUR J SURG ONCOL
- Weeraratne SD, 2012, ACTA NEUROPATHOL, V123, P539, DOI 10.1007/s00401-012-0969-5
- Wellner U, 2009, NAT CELL BIOL, V11, P1487, DOI 10.1038/ncb1998
- Williams LV, 2013, PLOS ONE, V8, DOI 10.1371/journal.pone.0083991
- Xu G, 2010, PLOS ONE, V5, DOI 10.1371/journal.pone.0015519
- Yang J, 2004, CELL, V117, P927, DOI 10.1016/j.cell.2004.06.006
- Yuen HF, 2007, HISTOPATHOLOGY, V50, P648, DOI 10.1111/j.1365-2559.2007.02665.x
- Zhang JC, 2012, BIOCHEM BIOPH RES CO, V417, P1100, DOI 10.1016/j.bbrc.2011.12.121
- Zhu ML, 2010, FASEB J, V24, P769, DOI 10.1096/fj.09-136994