Cytotoxin-Associated Gene A-Positive Helicobacter pylori Promotes Autophagy in Colon Cancer Cells by Inhibiting miR-125b-5p. (2nd March 2021)

• Record Type: Journal Article
• Authors: Zhong, Xiaolin; Chen, Ou; Zhou, TieJun; Lü, Muhan; Wan, Juyi
• Other Names: Chen Tingtao Academic Editor.
• Is Part Of: Canadian journal of infectious diseases & medical microbiology =. Volume 2021(2021)
• Publication Date: 2021-03-02
• Subjects: Communicable diseases -- Periodicals; Infection -- Periodicals; Communicable diseases; Infection; Communicable Diseases; Communicable Disease Control; Electronic journals; Periodicals; Fulltext; Internet Resources; Periodicals; 616.9
• DOI: 10.1155/2021/6622092
• Languages: English
• ISSNs: 1712-9532

Abstract

Abstract : Objectives . To investigate the effects of cytotoxin-associated gene A- (CagA-) positive Helicobacter pylori on proliferation, invasion, autophagy, and expression of miR-125b-5p in colon cancer cells. Methods . Colon cancer cells were cocultured with H. pylori (CagA+) to analyze the effects of H. pylori on miR-125b-5p and autophagy. Colon cancer cells infected with H. pylori (CagA+) were mimicked by transfection of CagA plasmid. The effects of CagA on the proliferation, invasion, and autophagy of colon cancer cells were analyzed. Cell counting kit-8 (CCK-8), clone formation, and Transwell assays were used to detect cell viability, proliferation, and invasion ability, respectively. Proteins and miRNAs were detected by western blotting and qPCR, respectively. Results . H. pylori (CagA+) inhibited expression of miR-125b-5p and promoted autophagy in colon cancer cells. MiR-125 b-5p was underexpressed in colon cancer cells after CagA overexpression. CagA promoted colon cancer cell proliferation, invasion, and autophagy. Overexpression of miR-125b-5p inhibited the proliferation, invasion, and autophagy of colon cancer cells and reversed the effects of CagA. Conclusion . H. pylori (CagA+) infection may promote the development and invasion of colon cancer by inhibiting miR-125b-5p.