LncRNA-LINC00152 down-regulated by miR-376c-3p restricts viability and promotes apoptosis of colorectal cancer cells.

Recent studies have demonstrated that the crucial regulatory roles of long noncoding RNAs (lncRNAs) in tumorigenesis. Expression levels of several lncRNAs are abnormally up-regulated or down-regulated and play a primary role in colorectal cancer (CRC) cell tumorigenesis. However, the potential role and regulatory mechanisms of the novel human lncRNA, LINC00152, in CRC cells are poorly understood. Here, we found that LINC00152 expression was significantly decreased in CRC tissues and CRC cell lines, and this change was more frequent in patients with advanced stage (tumor-node-metastasisi (TNM) III and IV). Overexpression of LINC00152 (LINC000152^over) resulted in decreased cell viability and increased apoptosis in CSC cell lines (HT-29 and SW480). Furthermore, decreased Ki-67 and B-cell lymphoma-2 (Bcl-2), and increased Fas, were observed in CSC cells. However, a change in Bax expression was undetected. Interestingly, microRNA (miR)-376c-3p down-regulated the expression of LINC00152 in CSC cells. Overexpression of miR-376c-3p (miR-376c-3p^over) enhanced viability and limited apoptosis of CSC cells. In addition, miR-376c-3p^over suppressed the effect of LINC00152^over on the viability and apoptosis of CSC cells. Taken together, these data indicate that LINC00152 in CSC cells negatively regulated by miR-376c-3p, restricts cell viability and stimulates cell apoptosis, possibly by modulating the expression of Ki-67, Bcl-2, and Fas. MiR-376c-3p/LINC00152 plays an important role in the pathogenesis of CRC and may serve as a potential target for its diagnosis and treatment.