Revista espanola de enfermedades digestivas · 2025
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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Huang Yesheng, Gong Chaofan, Wang Yu, Zhang Yichuan, Cen Meini
Аннотация
BACKGROUND: atrophic gastritis has a 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.
OBJECTIVE: this study evaluated the significance of miR-1260b in early gastric cancer and the progression of atrophic gastritis to gastric cancer aiming to explore a reliable biomarker.
MATERIALS AND METHODS: 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 to distinguish early gastric cancer was evaluated by ROC. In vitro, gastric cancer cells were infected with Helicobacter pylori (H. pylori), and the regulatory effect of miR-1260b on cell growth and metastasis was evaluated by CCK8 and Transwell assay.
RESULTS: 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 had higher miR-1260b levels, 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 alleviated these effects. miR-1260b negatively regulated ZNF302, and the knockdown of ZNF302 reversed the protective effect of miR-1260 knockdown on gastric cancer cells.
CONCLUSION: increasing miR-1260b can assist in the early diagnosis of gastric cancer and predict the risk of gastric cancer in atrophic gastritis patients. Silencing miR-1260b may alleviate the promotion of gastric cancer induced by H. pylori via negative modulation of ZNF302.
OBJECTIVE: this study evaluated the significance of miR-1260b in early gastric cancer and the progression of atrophic gastritis to gastric cancer aiming to explore a reliable biomarker.
MATERIALS AND METHODS: 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 to distinguish early gastric cancer was evaluated by ROC. In vitro, gastric cancer cells were infected with Helicobacter pylori (H. pylori), and the regulatory effect of miR-1260b on cell growth and metastasis was evaluated by CCK8 and Transwell assay.
RESULTS: 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 had higher miR-1260b levels, 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 alleviated these effects. miR-1260b negatively regulated ZNF302, and the knockdown of ZNF302 reversed the protective effect of miR-1260 knockdown on gastric cancer cells.
CONCLUSION: increasing miR-1260b can assist in the early diagnosis of gastric cancer and predict the risk of gastric cancer in atrophic gastritis patients. Silencing miR-1260b may alleviate the promotion of gastric cancer induced by H. pylori via negative modulation of ZNF302.