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.

Highlights

  • Colon cancer is a common digestive tract tumor that usually occurs in people aged 40–50 years

  • Teimoorian et al found that H. pylori is associated with colon cancer and adenomatous polyps [10]. e genotype differences of H. pylori strains are important factors leading to different clinical outcomes after infection. ere is a higher risk of serious clinical consequences of infection with cytotoxinassociated gene A- (CagA-) positive H. pylori than with the negative strain [11,12,13]

  • After coculture with H. pylori (CagA+), miR-125b-5p expression was significantly decreased in both DLD-1 (Figure 1(c)) and SW620 (Figure 1(d)) cells. e expression of the autophagy-related proteins LC3B-II/LC3B-I and Beclin-1 was significantly higher than that in the control group for both DLD-1 (Figure 1(e)) and SW620 (Figure 1(f )) cells. e results indicated that H. pylori (CagA+) inhibited the expression of miR-125b-5p and promoted the expression of LC3B-II/LC3B-I and Beclin-1 in colon cancer cells

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Summary

Introduction

Colon cancer is a common digestive tract tumor that usually occurs in people aged 40–50 years. Colon cancer is one of the most common tumors in China, and survey statistics show that the incidence of colon cancer among young people is increasing [1,2,3]. More than 50% of patients with colon cancer have distant metastasis at diagnosis, which is an important factor leading to poor prognosis [4, 5]. It has been found that H. pylori may be associated with the pathogenesis of colon cancer and polyps. Zumkeller et al first discovered through metastasis analysis that H. pylori infection is potentially linked to the pathogenesis of colon

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