LncRNA SNHG1 influences cell proliferation, migration, invasion, and apoptosis of non‐small cell lung cancer cells via the miR‐361‐3p/FRAT1 axis

摘要

BACKGROUND:Non-small-cell lung cancer (NSCLC) is the most lethal type of cancer. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) have been identified as crucial regulators in the development of NSCLC. The aim of our study was to explore the molecular mechanism of SNHG1 to enable better treatment for NSCLC patients.METHODS:Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression of Small nucleolar RNA host gene 1 (SNHG1), miR-361-3p and frequently rearranged in advanced T-cell lymphomas 1 (FRAT1). The protein level of FRAT1 was measured by western blot assay. Cell proliferation was evaluated by methyl thiazolyl tetrazolium (MTT) assay. Cell apoptosis was assessed by flow cytometry assay. The number of migrated and invaded cells were counted by transwell assay. The relationship between miR-361-3p and SNHG1 or FRAT1 was confirmed by dual-luciferase reporter assay.RESULTS:Our results indicated that SNHG1 and FRAT1 were highly expressed in NSCLC tissues and cells. SNHG1 silencing inhibited proliferation, induced apoptosis and blocked migration and invasion of NSCLC cells. Also, FRAT1 downregulation suppressed proliferation, promoted apoptosis and hindered migration and invasion of NSCLC cells. Further, FRAT1 could recover the effects of SNHG1 silencing on proliferation, apoptosis, migration and invasion of NSCLC cells. SNHG1 sponged miR-361-3p and negatively regulated miR-361-3p expression. Meanwhile, miR-361-3p targeted FRAT1 and inversely modulated FRAT1 expression. In addition, miR-361-3p inhibition abated the effect of SNHG1 knockdown on FRAT1 expression.CONCLUSION:In conclusion, LncRNA SNHG1 promoted the proliferation, repressed apoptosis and enhanced migration and invasion of NSCLC cells by regulating FRAT1 expression via sponging miR-361-3p.? 2019 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd.