Overexpression of LINC00691 promotes the proliferation and invasion of gastric cancer cells via the Janus kinase/signal transducer and activator of transcription signalling pathway

Abstract

This report aims to explore how LINC00691 regulates the proliferation and invasion of gastric cancer (GC). Clinical tissue and serum samples, as well as specimens in the Cancer Genome Atlas (TCGA) database, were used to analyse the expression of LINC00691 in GC. Our data indicated that the expression of LINC00691 in GC was significantly higher than that in healthy controls and was associated with clinicopathological features and survival time. In the GC cell lines MKN-45 and HGC-27, the knockdown of LINC00691 suppressed proliferation, colony formation, migration, and invasion. Bioinformatics analysis and luciferase reporter gene experiments showed that LINC00691 activated Lin28 transcription. Western blot analysis indicated that the knockdown of LINC00691 contributed to the decreased expression of p-JAK2 and p-STAT3 in GC cells. The Janus kinase/signal transducer and activator of transcription (JAK/STAT) signalling pathway inhibitor ruxolitinib effectively suppressed the effects of LINC00691. In addition, both LINC00691 and Lin28 promoted the expression of epidermal growth factor (EGF). Therefore, our study clarified that LINC00691 is highly expressed in GC and is a potential biomarker for GC diagnosis and prognosis. LINC00691 promotes the proliferation and invasion of GC cells by activating Lin28 transcription and facilitating EGF expression through the JAK/STAT signalling pathway, which provides new ideas for targeted therapy of GC.

Keywords: Biomarker; Gastric cancer; Lin28; Signalling pathway; lncRNA.