Long noncoding RNA-LET, which is repressed by EZH2, inhibits cell proliferation and induces apoptosis of nasopharyngeal carcinoma cell.

Recent studies have reported that long noncoding RNAs (lncRNAs) play critical roles in carcinogenesis and progression. LncRNA-LET, a recently identified lncRNA, has been shown to be a tumor suppressor in hepatocellular carcinoma. However, the expression and functional of lncRNA-LET in other type of cancers remain largely unknown. In this study, we found that lncRNA-LET was significantly downregulated in nasopharyngeal carcinoma (NPC) tissues compared with corresponding normal tissues. Decreased LET expression is significantly correlated with advanced clinical stage, larger tumor size, increased lymph node tumor burden, and poor survival of NPC patients. Gain- and loss-of-function experiments demonstrated that enhanced LET expression inhibited NPC cells proliferation and induced cell apoptosis. By contrast, the knockdown of LET promoted NPC cells proliferation and inhibited cell apoptosis. Importantly, we found lncRNA-LET is transcriptional repressed by EZH2-mediated H3K27 histone methylation on the LET promoter. The expressions of EZH2 and lncRNA-LET are significantly inversely correlated in NPC tissues. Collectively, these findings indicate a pivotal role for lncRNA-LET in NPC cell proliferation and apoptosis, and reveal an epigenetic mechanism for lncRNA-LET dysregulation.