Down-regulation of miR-221 inhibits proliferation of pancreatic cancer cells through up-regulation of PTEN, p27(kip1), p57(kip2), and PUMA.

Pancreatic cancer is the fourth leading cause of cancer related death in the US and exhibits aggressive features with short survival rate and high mortality. Therefore, it is important to understand the molecular mechanism(s) involved in the aggressive growth of pancreatic cancers, and further design novel targeted therapies for its treatment with better treatment outcome. In the present study, we found that the expression of miR-221 was significantly up-regulated in pancreatic cancer cell lines and tumor tissues compared to normal pancreatic duct epithelial cells and normal pancreas tissues.

Inactivation of AR and Notch-1 signaling by miR-34a attenuates prostate cancer aggressiveness.

Prostate cancer (PCa) is the second leading cause of cancer related death in men in the United States, suggesting that novel molecular targets as well as the development of agents that could deregulate such targets would become newer therapeutic approach for the treatment of castrate resistant prostate cancer (CRPC) especially the metastatic CRPC (mCRPC). In search for novel targets, microRNAs (miRNAs) are becoming an emerging area because miRNAs function as regulators of gene expression in human cancers including PCa. Previous studies from our laboratory have shown that the expression of miR-34a is significantly down-regulated in human PCa specimens consistent with PCa cell lines with aggressive characteristics, and that the silencing of miR-34a expression was in part due to hypermethylation of its promoter.