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논문 기본 정보

자료유형
학술저널
저자정보
Luo Juan (The First Affiliated Hospital of Kunming Medical University) Bai Luyan (The People’s Hospital of Mengzi) Tao Jun (Kunming Medical University) Wen Yu (The First Affiliated Hospital of Kunming Medical University) Li Mingke (The First Affiliated Hospital of Kunming Medical University) Zhu Yunzhen (The First Affiliated Hospital of Kunming Medical University) Luo Sufeng (The First Affiliated Hospital of Kunming Medical University) Pu Guangyu (The First Affiliated Hospital of Kunming Medical University) Ma Lanqing (The First Affiliated Hospital of Kunming Medical University)
저널정보
한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.10
발행연도
2021.10
수록면
1,223 - 1,230 (8page)
DOI
10.1007/s13258-021-01151-7

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Background Vacuolating cytotoxin (VacA) is an important virulence factor of Helicobacter pylori (H. pylori). It was previously believed that VacA can trigger the cascade of apoptosis on mitochondria to lead to cell apoptosis. Recently, it was found that VacA can induce autophagy. However, the molecular mechanism by which VacA induces autophagy is largely unknown. Objective We aimed to explore the molecular mechanism of autophagy induced by H. pylori in gastric cancer cells and the efect of autophagy on the survival of gastric cancer cells. Methods The autophagy of human gastric cancer cell line SGC7901 was detected by Western blot and RT-PCR in the treatment of VacA protein of H. pylori. The relationship between autophagy and reactive oxygen species (ROS) in the proliferation of gastric cancer cells were studied by gene expression silences (siRNA) and CM-H2DCFDA (DCF) staining. Results The results showed that VacA protein secreted by H. pylori in the supernatant stimulated autophagy in SGC7901 cells. After VacA protein treatment, the mRNA expressions of BECN1, ATG7 and PIK3C3, were up-regulated. ATG7 silencing by siRNA inhibited VacA-induced autophagy. Furthermore, our data demonstrated that VacA protein increased ROS levels. Addition of the antioxidant N-acetyl-l-cysteine (NAC) suppressed the levels of ROS, leading to inhibition of autophagy. Conclusions H. pylori VacA is a key toxin that induces autophagy by increased ROS levels. And our fndings demonstrated that VacA signifcantly inhibited proliferation in SGC7901 cells.

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