Tumor relapse after therapy typifies @entity157 ( @entity157 ) and is believed to be attributable to @entity5 stem cells (CSCs) that survive treatment. We have previously identified a CSC population derived from @entity157 that is characterized by @entity5439 . Despite our growing knowledge of the importance of this subset of cells in driving @entity157 , the regulatory mechanism of @entity5439 is not known. Epigenetic changes are believed to be essential in the control of @entity5 and stem cells. Here, we report the epigenetic regulation of @entity5439 by miR-142-3p. The interaction between @entity5439 and miR-142-3p was identified by in silico prediction and substantiated by luciferase reporter analysis. Expression of @entity5439 was found to be inversely correlated with miR-142-3p in @entity157 clinical samples as well as in cell lines. Importantly, lower miR-142-3p expression in @entity157 was significantly associated with worst survival. Functional studies with miR-142-3p stably transduced in @entity157 cells demonstrated a diminished ability to self-renew, initiate @entity5 growth, invade, migrate, induce angiogenesis and resist chemotherapy. Rescue experiments whereby @entity5439 and miR-142-3p is simultaneously overexpressed compensated the deregulated ability of the cells to confer these features. Thus, miR-142-3p directly targets @entity5439 to regulate its ability to confer @entity5 and stem cell-like features in @entity157 .

Regulatory role of miR-142-3p on the functional hepatic cancer stem cell marker XXXX .

@entity5 :: ('MESH:D009369', 'Disease') :: ['tumor', 'residual cancer', 'cancer'] @entity157 :: ('MESH:D006528', 'Disease') :: ['HCC', 'hepatocellular carcinoma'] @entity5439 :: ('8842', 'Gene') :: ['CD133']
@entity5439 :: (8842,Gene) :: ['CD133']
