Long non-coding RNA OECC promotes cell proliferation and metastasis through the PI3K/Akt/mTOR signaling pathway in human lung cancer.

Abstract

Lung cancer is one of the most common malignancies worldwide; however, its detailed molecular mechanism remains largely unknown. Long non-coding RNAs (lncRNAs) have been identified to serve critical roles in tumorigenesis. The aim of the present study was to investigate the role of a newly identified lncRNA, overexpressed in colorectal cancer (OECC), in human lung cancer. It was initially revealed that the relative transcript level of OECC was highly upregulated in clinical human lung cancer tissues as well as in cultured lung cancer cells. Knockdown of OECC with specific short hairpin RNAs in lung cancer cell lines A549 and 95D inhibited colony formation and cell viability, as evidenced using colony formation assays and cell proliferation assays. Furthermore, depletion of OECC in A549 and 95D cells suppressed migration and invasion, which was verified using Transwell assays. RNA-sequence analysis suggested that the phosphoinositide 3-kinase/protein kinase B (Akt)/mammalian target of rapamycin signaling pathway was positively regulated by OECC in lung cancer cells A549. In addition, overexpression of Akt in OECC-depleted A549 and 95D cells reversed the suppression of proliferation and migration caused by OECC depletion. The results of the present study identified lncRNA OECC as a novel regulator of lung cancer progression and provided new clues for the clinical treatment of lung cancer.