Abstract
MicroRNAs, non-coding 20–22 nucleotide single-stranded RNAs, result in translational repression or degradation and gene silencing of their target genes, and significantly contribute to the regulation of gene expression. In the current study, we report that miR-182 expression was significantly upregulated in prostate cancer tissues and four cell lines, compared to benign prostatic hyperplasia tissues and normal prostatic epithelial (RWPE-1) cells. Ectopic overexpression of miR-182 significantly promotes the proliferation, increases the invasion, promotes the G1/S cell cycle transition and reduces early apotosis of PC-3 cells, while suppression of miR-182 decreased the proliferation and invasion, inhibits the G1/S cell cycle transition and increase early apotosis of PC-3 cells. Additionally, we demonstrated that miR-182 could downregulate expression of NDRG1 by directly targeting the NDRG1 3′-untranslated region. In conclusion, our results suggest that miR-182 plays an important role in the proliferation of human prostate cancer cells by directly suppressing the tumor supressor gene NDRG1. We uncovered a new epigenetic regulation of NDRG1.
Highlights
Prostate cancer (PCa) continues to be one of the biggest health problems for the aging male, with an estimated 238,590 new cases and 29,720 cancer related deaths expected in 2013 in the United States alone [1]
We demonstrated that miR-182 promoted PCa PC-3 cells proliferation and invasion by directly targeting the 39-untranslated region (UTR) of N-myc downstream regulated gene 1 (NDRG1, NM_006096.3) mRNA
MiR-182 was Upregulated in PCa Cell Lines Real-time RT-PCR analysis revealed that miR-182 expression was markedly increased in four common PCa cell lines tested (PC3, DU145, 22Rv1 and LNCaP), compared to normal prostate epithelial RWPE-1 cell, indicating that miR-182 is upregulated in PCa cell lines and PC-3 has the highest expression level (Figure 2)
Summary
Prostate cancer (PCa) continues to be one of the biggest health problems for the aging male, with an estimated 238,590 new cases and 29,720 cancer related deaths expected in 2013 in the United States alone [1]. Therapy for unconfined tumors still represents a major problem Standard treatment for these patients is antiandrogens to achieve total androgen blockade [2]. That tumors progress and circumvent the treatment is a very frequent event and there are no effective treatments for castration resistant PCa (CRPC) patients, though urologist are trying to use chemotherapeutics. Both genetic and environmental factors are considered to be major factors, the molecular mechanisms of PCa development and progression remain largely unknown.better understanding the pathogenesis of PCa and exploring novel intervention targets for PCa are urgently demanding tasks
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