Glucose-6 phosphatase catalytic subunit inhibits the proliferation of liver cancer cells by inducing cell cycle arrest.
10.3760/cma.j.cn501113-20210204-00067
- Author:
Xue LIN
1
;
Xuan Ming PAN
1
;
Zi Ke PENG
2
;
Kai WANG
1
;
Ni TANG
1
Author Information
1. The Key Laboratory of Molecular Biology for Infectious Diseases (Ministry of Education), Chongqing 400016, China.
2. Chongqing Yucai Middle School, Chongqing 400050, China.
- Publication Type:Journal Article
- Keywords:
Cell cycle;
Cell proliferation;
Glucose-6 phosphatase catalytic subunit;
Hepatocellular carcinoma
- MeSH:
Catalytic Domain;
Cell Cycle Checkpoints;
Cell Line, Tumor;
Cell Proliferation;
Gene Expression Regulation, Neoplastic;
Glucose-6-Phosphatase/metabolism*;
Humans;
Liver Neoplasms/genetics*
- From:
Chinese Journal of Hepatology
2022;30(2):213-219
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of glucose-6-phosphatase catalytic subunit (G6PC) recombinant adenovirus on proliferation and cell cycle regulation of liver cancer cells. Methods: Recombinant adenovirus AdG6PC was constructed. Huh7 cells and SK-Hep1 cells were set as Mock, AdGFP and AdG6PC group. Cell proliferation and clone formation assay were used to observe the proliferation of liver cancer cells. Transwell and scratch assay were used to observe the invasion and migration of liver cancer cells. Cell cycle flow cytometry assay was used to analyze the effect of G6PC overexpression on the proliferation cycle of liver cancer cells. Western blot was used to detect the effect of G6PC overexpression on the cell-cycle protein expression in liver cancer cells. Results: The recombinant adenovirus AdG6PC was successfully constructed. Huh7 and SK-Hep1 cells proliferation assay showed that the number of proliferating cells in the AdG6PC group was significantly lower than the other two groups (P < 0.05). Clone formation assay showed that the number of clones was significantly lower in AdG6PC than the other two groups (P < 0.05), suggesting that G6PC overexpression could significantly inhibit the proliferation of liver cancer cells. Transwell assay showed that the number of cell migration was significantly lower in AdG6PC than the other two groups (P < 0.05). Scratch repair rate was significantly lower in AdG6PC than the other two groups (P < 0.05), suggesting that G6PC overexpression can significantly inhibit the invasion and migration of liver cancer cells. Cell cycle flow cytometry showed that G6PC overexpression had significantly inhibited the Huh7 cells G(1)/S phase transition. Western blot result showed that G6PC overexpression had down-regulated the proliferation in cell-cycle related proteins expression. Conclusion: G6PC inhibits the proliferation, cell-cycle related expression, and migration of liver cancer cells by inhibiting the G(1)/S phase transition.
