Helicobacter pylori promotes gastric cancer metastasis via up-regulating the expression of Bmi-1.
- Author:
Xiaolei TANG
1
;
Ying HUA
2
;
Sheng LI
3
;
Baijing DING
4
Author Information
1. Department of Translational Medicine Centre, the Second Affiliated Hospital, Wannan Medical College, Wuhu 241000, China.
2. School of Nursing, Wannan Medical College, Wuhu 241000, China. *Corresponding author, E-mail: 764857482@qq.com.
3. Department of Gastroenterology, Wuhu Second People's Hospital, Wuhu 241000, China.
4. Department of Gastroenterology, Wuhu First People's Hospital, Wuhu 241000, China.
- Publication Type:Journal Article
- MeSH:
Humans;
Cell Line, Tumor;
Helicobacter Infections/genetics*;
Helicobacter pylori;
Lymphatic Metastasis;
Retrospective Studies;
Stomach Neoplasms/pathology*;
Polycomb Repressive Complex 1/genetics*
- From:
Chinese Journal of Cellular and Molecular Immunology
2023;39(6):532-538
- CountryChina
- Language:Chinese
-
Abstract:
Objective To clarify whether Helicobacter pylori (H. pylori) can promote metastasis of gastric cancer cells via the high-expression of induced B cell specific Moloney murine leukemia virus integration site 1 (Bmi-1). Methods The gastric cancer tissue specimens from 82 patients were collected for this study. The protein and gene expression level of Bmi-1 in gastric adenocarcinoma tissue were detected by immunohistochemistry and real time quantitative PCR, respectively. And meanwhile the correlation between Bmi-1 levels and pathological features, and prognosis of gastric cancer were analyzed retrospectively. Then, the GES-1 cells were transfected with pLPCX-Bmi-1 plasmid and infected with H. pylori respectively. After the Bmi-1 overexpression in GES-1 cells, the invasion ability of the GES-1 cells was detected by Transwell assay, and the cell cycle and apoptosis were detected by flow cytometry. Results The mRNA and protein of Bmi-1 expression in gastric cancer tissues were higher than tumor-adjacent tissue, and the high expression of Bmi-1 was positively correlated with tumor invasion, TNM stage, tumor differentiation, lymph node metastasis and H. pylori infection. When expression of Bmi-1 was up-regulated as a result of H.pylori infection or pLPCX-Bmi-1 transfection, the GES-1 cells had higher invasiveness and lower apoptosis rate with the above treatment respectively. Conclusion H. pylori infection can inhibit the apoptosis of gastric cancer cells and promote their invasion via up-regulating expression of Bmi-1.
