LncRNA abrogation inhibits proliferation and induces apoptosis in esophageal adenocarcinoma cells via activation of the STAT3/c-Myc/FAK signaling.

Long non-coding RNAs (lncRNAs) have involved in human malignancies and played an important role in gene regulations. The dysregulation of lncRNA has been reported in several cancers. However, the role of in esophageal adenocarcinoma (EAC) is poorly understood. Loss of function approaches were used to investigate the biological role of in EAC cells. The effects of on cell proliferation were evaluated by WST-1 and colony formation assays. The effects of on cell migration and invasion were examined using transwell assays. QRT-PCR and Western blot were used to evaluate the mRNA and protein expression of related genes. In this study, abrogation of inhibited cell proliferation, colony formation, invasion and migration in EAC 3 cell lines (OE33, OE19 and FLO-1). Mechanistically, silencing decreased the expression of STAT3/c-Myc/p-FAK proteins and induced apoptosis in EAC cell lines. These results delineate a novel mechanism of in EAC, and may provide potential targets by developing lncRNA-based therapies for EAC.