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Blocking effects of genistein on cell proliferation and possible mechanism in human gastric carcinoma
Hong-Bin Cui1, Xiao-Lin Na, Dan-Feng Song
1Department of Food Nutrition and Hygiene, Public Health College, Harbin Medical University, Harbin 150001, Heilongjiang Province, China. cuihb_h@public.hr.hl.cn
Aim:
To study the blocking effects of genistein on cell proliferation cycle in human gastric carcinoma cells (SGC-7901) and the possible mechanism.
Methods:
MTT assay was applied in the detection of the inhibitory effects of genistein on cell proliferation. Flow cytometry was used to analyze the cell cycle distribution. Immunocytochemical technique and Western blotting were performed to detect the protein expression of cyclin D1, cyclin B1 and p21(waf1/cip1).
Results:
Genistein significantly inhibited the growth and proliferation of human gastric carcinoma cells (SGC-7901). Seven days after treatment with different concentrations of genistein (2.5, 5.0, 10.0, 20.0 microg/mL), the growth inhibitory rates were 11.2%, 28.8%, 55.3%, 84.7% respectively and cell cycles were arrested at the G(2)/ M phase. Genistein decreased cyclin D1 protein expression and enhanced cyclin B1 and p21(waf/cip1) protein expression in a concentration-dependent manner.
Conclusion:
The growth and proliferation of SGC-7901 cells can be inhibited by genistein via blocking the cell cycle, with reduced expression of cyclin D1 and enhanced expression of cyclin B1 and p21(waf/cip1) protein in the concentration range of 0-20 microg/mL.
Insights
Genistein effectively inhibits human gastric carcinoma cell growth by arresting the cell cycle at G2/M phase. This mechanism involves downregulating cyclin D1 and upregulating cyclin B1 and p21(waf1/cip1) protein expression.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Gastric carcinoma is a significant global health concern.
- Understanding cell proliferation mechanisms is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the effects of genistein on the cell cycle of human gastric carcinoma cells (SGC-7901).
- To elucidate the underlying molecular mechanisms of genistein's anti-proliferative action.
Main Methods:
- MTT assay for assessing cell proliferation inhibition.
- Flow cytometry for cell cycle distribution analysis.
- Immunocytochemistry and Western blotting for detecting key cell cycle protein expression (cyclin D1, cyclin B1, p21(waf1/cip1)).
Main Results:
- Genistein demonstrated significant dose-dependent inhibition of SGC-7901 cell growth and proliferation.
- Cell cycle arrest at the G(2)/M phase was observed following genistein treatment.
- Genistein modulated the expression of cell cycle regulatory proteins, decreasing cyclin D1 and increasing cyclin B1 and p21(waf1/cip1).
Conclusions:
- Genistein effectively inhibits SGC-7901 cell proliferation by inducing cell cycle arrest.
- The observed effects are mediated by alterations in cyclin D1, cyclin B1, and p21(waf1/cip1) protein levels.
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