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circRNA_0006470 promotes the proliferation and migration of gastric cancer cells by functioning as a sponge of miR-27b-3p.

Authors :
Yejia CUI
Jin CAO
Shaolong HUANG
Jinjun YE
Haohai HUANG
Dan LIAO
Yufeng YANG
Aiping YIN
Wanchan CHEN
Yelin YAO
Yingai HE
Rong PU
Source :
Neoplasma; 2021, Vol. 68 Issue 6, p1245-1256, 12p
Publication Year :
2021

Abstract

Cancer pathogenesis is influenced by epigenetic alterations mediated by circular RNAs (circRNAs). In this study, we aimed to investigate the regulatory mechanisms and cytological function of hsa_circ_0006470/miR-27b-3p in gastric cancer (GC). circRNA and microRNA expressions in cancer cells were measured by the qRT-PCR method. A dual-luciferase reporter assay was performed to validate the binding of hsa_circ_0006470 with miR-27b-3p. hsa_circ_0006470 was silenced in AGS cells, and proliferation, migration, and invasion were tested via the CCK-8 assay and Transwell system, respectively. The autophagy in GC cells was assessed by marker protein detection and transmission electron microscope. The results showed that hsa_circ_0006470 expression was significantly elevated in GC cells, which was mainly distributed in cytoplasmic components and could directly bind with miR-27b-3p in GC cells. Silencing of hsa_circ_0006470 repressed cell proliferation, migration, and invasion, which may be through regulating miR-27b-3p/Receptor tyrosine kinase-like orphan receptor 1 (ROR1). Silencing of hsa_circ_0006470 also elevated LC3II and Beclin-1 and suppressed p62 protein abundances, which subsequently induced autophagy in AGS cells. Furthermore, we found that hsa_circ_0006470 promotes phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha (PI3KCA) expressing by sponging miR-27b-3p. In conclusion, hsa_circ_0006470 promoted GC cell proliferation and migration through targeting miR-27b-3p and suppressing autophagy machinery. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
00282685
Volume :
68
Issue :
6
Database :
Complementary Index
Journal :
Neoplasma
Publication Type :
Academic Journal
Accession number :
155277956
Full Text :
https://doi.org/10.4149/neo_2021_210222N235