Increasing miR-1260b predicts the risk of gastric cancer in atrophic gastritis patients and regulates cell growth and metastasis of gastric cancer.

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Atrophic gastritis is of high risk of progressing to gastric cancer. Screening early gastric cancer and predicting the risk of atrophic gastritis developing into gastric cancer could improve the prognosis of gastric cancer. This study evaluated the significance of miR-1260b in early gastric cancer and in the progression of atrophic gastritis to gastric cancer aiming to explore a reliable biomarker. The study enrolled 78 early gastric cancer patients and 77 atrophic gastritis patients. The expression of miR-1260b was detected in serum and tissue samples by PCR. The risk of atrophic gastritis patients progressing to gastric cancer was assessed and correlated with miR-1260b levels. The potential of miR-1260b in distinguishing early gastric cancer was evaluated by ROC. In vitro, gastric cancer cells were infected with Helicobacter pylori, and the regulatory effect of miR-1260b on cell growth and metastasis was evaluated by CCK8 and Transwell assay. Significant upregulation of miR-1260b was observed in early gastric cancer patients relative to atrophic gastritis patients, which distinguishes early gastric cancer patients and showed a positive correlation with the risk of atrophic gastritis patients developing gastric cancer. Early gastric cancer patients with positive H. pylori infection showed a higher miR-1260b level, and increasing miR-1260b was also observed in H. pylori-infected gastric cancer cells. H. pylori promoted cell growth and metastasis of gastric cancer while silencing miR-1260b could alleviate these effects. miR-1260b negatively regulated ZNF302, and the knockdown of ZNF302 reversed the protective effect of miR-1260 knockdown on gastric cancer cells. Increasing miR-1260b can assist diagnose early gastric cancer and predict the risk of gastric cancer in atrophic gastritis patients. Silencing miR-1260b could alleviate the promotion of gastric cancer induced by H. pylori via negatively modulating ZNF302.