2016•Jiefangjun yixue zazhiRequires access

Inhibitory effect of epigallocatechin-3-gallate on the proliferation of hepatic carcinoma cells

Shuai Wang, Zhimei Shang, Limin Huang, Liang Liu, Zhonglin Wu, Yang Zhao, Jingyan Zhu

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Abstract

Objective  To study the effect of epigallocatechin-3-gallate (EGCG) on the proliferation and apoptosis of hepatic carcinoma HepG2 cells, and to explore the possible mechanism. Methods  HepG2 cells were treated with EGCG in various concentrations (0, 25, 50, 100, 200, 400mg/L) for 24, 48 and 72h, and then the cell proliferation inhibition rate was determined with MTT. Again, the HepG2 cells were treated with various concentrations of EGCG (0, 50, 100, 200mg/L) for 24h, and then the cell apoptosis rate, cell cycle, and the expressions of cell division cycle protein 25A (CDC25A), and Smad3 protein were determined with flow cytometry. mRNA expressions of CDC25A and Smad3 were assessed with RT-PCR. Results  The results of MTT showed that various concentrations of EGCG inhibited the growth of HepG2 cells in dose and time dependent manner (P<0.01). The result of flow cytometry showed that, with the increase of of EGCG concentration, the cell proliferation index (PI) decreased significantly (P<0.01), while the apoptosis rate increased obviously (P<0.01); the expression levels of CDC25A protein and mRNA decreased (P<0.05) and of Smad3 protein and mRNA increased (P<0.05). Conclusion  EGCG may play a role in growth inhibition of hepatic carcinoma cells by down-regulating the expression of CDC25A, up-regulating the expression of Smad3, thus inhibiting proliferation and inducing apoptosis of HepG2 cells. DOI: 10.11855/j.issn.0577-7402.2016.03.06

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Objective  To study the effect of epigallocatechin-3-gallate (EGCG) on the proliferation and apoptosis of hepatic carcinoma HepG2 cells, and to explore the possible mechanism. Methods  HepG2 cells were treated with EGCG in various concentrations (0, 25, 50, 100, 200, 400mg/L) for 24, 48 and 72h, and then the cell proliferation inhibition rate was determined with MTT. Again, the HepG2 cells were treated with various concentrations of EGCG (0, 50, 100, 200mg/L) for 24h, and then the cell apoptosis rate, cell cycle, and the expressions of cell division cycle protein 25A (CDC25A), and Smad3 protein were determined with flow cytometry. mRNA expressions of CDC25A and Smad3 were assessed with RT-PCR. Results  The results of MTT showed that various concentrations of EGCG inhibited the growth of HepG2 cells in dose and time dependent manner (P<0.01). The result of flow cytometry showed that, with the increase of of EGCG concentration, the cell proliferation index (PI) decreased significantly (P<0.01), while the apoptosis rate increased obviously (P<0.01); the expression levels of CDC25A protein and mRNA decreased (P<0.05) and of Smad3 protein and mRNA increased (P<0.05). Conclusion  EGCG may play a role in growth inhibition of hepatic carcinoma cells by down-regulating the expression of CDC25A, up-regulating the expression of Smad3, thus inhibiting proliferation and inducing apoptosis of HepG2 cells. DOI: 10.11855/j.issn.0577-7402.2016.03.06

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Available abstract

Objective  To study the effect of epigallocatechin-3-gallate (EGCG) on the proliferation and apoptosis of hepatic carcinoma HepG2 cells, and to explore the possible mechanism. Methods  HepG2 cells were treated with EGCG in various concentrations (0, 25, 50, 100, 200, 400mg/L) for 24, 48 and 72h, and then the cell proliferation inhibition rate was determined with MTT. Again, the HepG2 cells were treated with various concentrations of EGCG (0, 50, 100, 200mg/L) for 24h, and then the cell apoptosis rate, cell cycle, and the expressions of cell division cycle protein 25A (CDC25A), and Smad3 protein were determined with flow cytometry. mRNA expressions of CDC25A and Smad3 were assessed with RT-PCR. Results  The results of MTT showed that various concentrations of EGCG inhibited the growth of HepG2 cells in dose and time dependent manner (P<0.01). The result of flow cytometry showed that, with the increase of of EGCG concentration, the cell proliferation index (PI) decreased significantly (P<0.01), while the apoptosis rate increased obviously (P<0.01); the expression levels of CDC25A protein and mRNA decreased (P<0.05) and of Smad3 protein and mRNA increased (P<0.05). Conclusion  EGCG may play a role in growth inhibition of hepatic carcinoma cells by down-regulating the expression of CDC25A, up-regulating the expression of Smad3, thus inhibiting proliferation and inducing apoptosis of HepG2 cells. DOI: 10.11855/j.issn.0577-7402.2016.03.06

Key concepts: Apoptosis, Flow cytometry, Cell growth, Cell cycle, Molecular biology, Chemistry, Messenger RNA, MTT assay

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