J Cancer 2015; 6(3):292-301. doi:10.7150/jca.11038
Controlling RECK miR21 Promotes Tumor Cell Invasion and Is Related to Biochemical Recurrence in Prostate Cancer
Laboratory of Medical Research, LIM55, Urology Department, University of Sao Paulo Medical School, Sao Paulo, Brazil
The search for biomarkers to characterize prostate cancer aggressiveness has been the objective for the majority of researchers involved with the most prevalent tumor in men. MiRNAs are important for the control of many cellular functions and their deregulation is involved with tumor development and progression. To find miRNAs differentially expressed in prostate cancer and their relation to prognostic factors and biochemical recurrence we studied 53 surgical specimens from men who underwent radical prostatectomy, through a microarray analysis using the microarray platform (GeneChip® miRNA Array - Affymetrix) with more than 46,000 probes and 847 mature human miRNAs and transcripts. We defined different as an expression level greater or less than 1.1 with p<0.05. The validation study using qRT-PCR had confirmed miR21 as overexpressed in tumor that have recurred with a risk of 2.5. Transfection of miR-21 using lipid based assay in DU145 cell line, showed decrease in expression of RECK resulting in increase in expression of MMP9. Invasion assay with Matrigel showed increase in tumor cell invasion after miR-21 transfection. We conclude that miR-21 overexpression is related to increased biochemical recurrence after surgical treatment of prostate cancer. And the negative control of RECK results in overexpression of MMP9 promotes increasing tumor cell invasion supporting miR-21 as an oncomiR related to aggressiveness in prostate cancer.
Keywords: Prostate cancer, Micro RNA, Microarray, Biochemical recurrence, Prognosis, miR-21, Cell invasion, RECK, DU145
Leite KRM, Reis ST, Viana N, Morais DR, Moura CM, Silva IA, Pontes J Jr, Katz B, Srougi M. Controlling RECK miR21 Promotes Tumor Cell Invasion and Is Related to Biochemical Recurrence in Prostate Cancer. J Cancer 2015; 6(3):292-301. doi:10.7150/jca.11038. Available from http://www.jcancer.org/v06p0292.htm