Circ_0078767 suppresses non-small-cell lung cancer by protecting RASSF1A expression via sponging miR-330-3p.

Abstract:

OBJECTIVES:This study was designed to investigate the role of circ_0078767/miR-330-3p/RASSF1A in non-small-cell lung cancer (NSCLC). Bioinformatic analysis was performed to screen for the differentially expressed genes in NSCLC tissues from adjacent lung tissues. MATERIALS AND METHODS:qRT-PCR was used to detect the RNA expression of genes in cells and tissues, and Western blot was conducted to determine the protein levels of RASSF1A in tissues and cells. A miRanda algorithm was used to predict the targeted relationship among RNAs. A dual-luciferase reporter gene assay was conducted to verify the targeted relationship. Flow cytometry was performed to investigate the effects of circ_0078767/miR-330-3p/RASSF1A on cell cycle progression and apoptosis. A CCK-8 assay was conducted to explore the effects of circ_0078767/miR-330-3p/RASSF1A on cell proliferation. A transwell invasion assay was completed to study the effects of circ_0078767/miR-330-3p/RASSF1A on cell invasion. Lastly, an in vivo assay was conducted to investigate the effects of circ_0078767/miR-330-3p/RASSF1A on tumour development. RESULTS:Circ_0078767 and RASSF1A were downregulated, while miR-330-3p was upregulated in NSCLC tissues than that in adjacent tissues. miR-330-3p had a binding relationship with circ_0078767 and RASSF1A. The overexpression of circ_0078767 and RASSF1A or the underexpression of miR-330-3p significantly suppressed NSCLC cell viability, cell cycle progression and invasion while also significantly promoting cell apoptosis. Additionally, these modulations significantly suppressed in vivo tumour growth. CONCLUSIONS:Circ_0078767 could suppress NSCLC progression by inhibiting miR-330-3p, which thereby increased RASSF1 levels.

journal_name

Cell Prolif

journal_title

Cell proliferation

authors

Chen T,Yang Z,Liu C,Wang L,Yang J,Chen L,Li W

doi

10.1111/cpr.12548

subject

Has Abstract

pub_date

2019-03-01 00:00:00

pages

e12548

issue

2

eissn

0960-7722

issn

1365-2184

journal_volume

52

pub_type

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