已发表论文

Circ_0084927 通过海绵化 miR-142-3p 和上调 ARL2 促进宫颈癌的发展

 

Authors Chen L, Zhang X, Wang S, Lin X, Xu L

Received 2 June 2020

Accepted for publication 15 August 2020

Published 28 September 2020 Volume 2020:12 Pages 9271—9283

DOI https://doi.org/10.2147/CMAR.S263596

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 3

Editor who approved publication: Dr Seema Singh

Background: Cervical cancer is a fatal burden for women. Circular RNAs (circRNAs) are important regulators in cancer development. Our study aimed to investigate the function and action mechanism of a novel circRNA, circ_0084927, in cervical cancer.
Methods: The expression of circ_0084927, miR-142-3p and ADP-ribosylation factor-like protein 2 (ARL2) mRNA was measured by quantitative real-time polymerase chain reaction (qRT-PCR). For functional analyses, cell proliferation was assessed using cell counting kit-8 (CCK-8) assay. Cell cycle distribution was monitored by flow cytometry assay. Cell migration and cell invasion were evaluated by transwell assay. The interaction between miR-142-3p and circ_0084927 or ARL2 was predicted by the bioinformatics analysis and validated by dual-luciferase reporter assay and RNA immunoprecipitation assay (RIP) assay. The expression of ARL2 at the protein level was detected by Western blot. Animal tumor formation assay was performed to monitor the tumorigenicity of circ_0084927 in vivo.
Results: The expression of circ_0084927 and ARL2 was enhanced in cervical cancer tissues and cells, while the expression of miR-142-3p was opposite to them. Circ_0084927 knockdown significantly blocked cervical cancer cell proliferation, migration and invasion and induced cell cycle arrest. MiR-142-3p was targeted by circ_0084927, and miR-142-3p inhibition reversed the effects of circ_0084927 knockdown. Besides, miR-142-3p bound to ARL2, and the inhibitory effects of miR-142-3p restoration on cell proliferation, cycle, migration and invasion were counteracted by ARL2 overexpression. More importantly, circ_0084927 upregulated ARL2 expression by sponging miR-142-3p. Circ_0084927 knockdown retarded tumor growth in vivo by regulating miR-142-3p and ARL2.
Conclusion: Circ_0084927 accelerated the progression of cervical cancer partly by mediating the miR-142-3p/ARL2 axis.
Keywords: circ_0084927, miR-142-3p, ARL2, cervical cancer




Figure 6 ARL2 overexpression partly abolished the antitumor role of...