Silencing of LOC389641 impairs cell proliferation and induces autophagy via EGFR/MET signaling in lung adenocarcinoma

Abstract

High-throughput RNA-sequencing studies of tumor samples have identified a large number of long non-coding RNAs (lncRNAs) which are associated with various types of cancer. LncRNAs play key roles in regulating chromatin dynamics, gene expression, growth, differentiation and development. However, the role of <i>LOC389641</i> in non-small cell lung cancer (NSCLC) tumorigenesis is not clear. Here, we investigated the expression pattern, roles and mechanism of <i>LOC389641</i> in lung cancer. <i>LOC389641</i> expressions in tumor tissues and cell lines were measured by qRT-PCR. Functional studies including colony formation, cell proliferation and invasion were performed in lung cancer cell lines and Western blot was used to exam the protein changes upon siRNA treatment. We found that <i>LOC389641</i> was highly expressed in lung adenocarcinomas and was associated with poor patient survival. Silencing of <i>LOC389641</i> reduced colony formation, cell proliferation and invasion, as well as induced autophagy and apoptosis of lung adenocarcinoma cell lines <i>in vitro</i>. Mechanistically, downregulation of <i>LOC389641</i> was found to decrease EGFR, MET and STAT3 proteins expression in lung cancer cells. <i>LOC389641</i> is highly expressed and plays an oncogenic role in this type of NSCLC. Because of its specificity, <i>LOC389641</i> may be a potential biomarker for prognosis and a possible target for lung adenocarcinoma.