2015Shandong yiyaoRequires access

Effects of 17-AAG combined with cisplatin on proliferation and apoptosis of human hepatoma cell line HepG2

Jianqin Zhang

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Abstract

Objective To explore the effects of 17-AAG combined with cisplatin( DDP) on the proliferation of human hepatocellular carcinoma Hep G2 cells and its mechanism. Methods Hep G2 cells in the logarithmic phase were divided into the control group and groups A,B and C. The control group was only added with medium. Group A was added with0. 625 μmol / L 17-AAG,group B was added with 1. 0 μg / m L DDP,and group C was added with 0. 625 μg / m L 17-AAG and 1. 0 μg / m L DDP. After being cultured for 24 h and 48 h,the cell proliferation inhibition rates of groups A,B and C were determined by MTT,the apoptosis rate was measured by flow cytometry,and the Bax and Bcl-2 mRNA in each group was measured by RT-PCR. Results The cell proliferation inhibition rates of groups A,B and C which were cultured for 48 h were all higher than those of being cultured for 24 h( all P 0. 05),the cell proliferation inhibition rate of group C was higher than those of groups A and B at the same time of culture( all P 0. 05). After being cultured for 48 h,the apoptosis rate and Bax mRNA in the groups A,B and C were higher than that of the control group,while Bcl-2 mRNA was lower than that of the control group( all P 0. 05); the apoptosis rate and Bax mRNA of group C were higher than those of groups A and B,but the Bcl-2 mRNA was lower than those of groups A and B( all P 0. 05). Conclusions 17-AAG inhibits the growth of human hepatocellular carcinoma Hep G2 cells and has synergistic effect with cisplatin. The mechanism may be related to the up-regulation of Bax mRNA and down-regulation of Bcl-2 mRNA expression.

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Objective To explore the effects of 17-AAG combined with cisplatin( DDP) on the proliferation of human hepatocellular carcinoma Hep G2 cells and its mechanism. Methods Hep G2 cells in the logarithmic phase were divided into the control group and groups A,B and C. The control group was only added with medium. Group A was added with0. 625 μmol / L 17-AAG,group B was added with 1. 0 μg / m L DDP,and group C was added with 0. 625 μg / m L 17-AAG and 1. 0 μg / m L DDP. After being cultured for 24 h and 48 h,the cell proliferation inhibition rates of groups A,B and C were determined by MTT,the apoptosis rate was measured by flow cytometry,and the Bax and Bcl-2 mRNA in each group was measured by RT-PCR. Results The cell proliferation inhibition rates of groups A,B and C which were cultured for 48 h were all higher than those of being cultured for 24 h( all P 0. 05),the cell proliferation inhibition rate of group C was higher than those of groups A and B at the same time of culture( all P 0. 05). After being cultured for 48 h,the apoptosis rate and Bax mRNA in the groups A,B and C were higher than that of the control group,while Bcl-2 mRNA was lower than that of the control group( all P 0. 05); the apoptosis rate and Bax mRNA of group C were higher than those of groups A and B,but the Bcl-2 mRNA was lower than those of groups A and B( all P 0. 05). Conclusions 17-AAG inhibits the growth of human hepatocellular carcinoma Hep G2 cells and has synergistic effect with cisplatin. The mechanism may be related to the up-regulation of Bax mRNA and down-regulation of Bcl-2 mRNA expression.

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Available abstract

Objective To explore the effects of 17-AAG combined with cisplatin( DDP) on the proliferation of human hepatocellular carcinoma Hep G2 cells and its mechanism. Methods Hep G2 cells in the logarithmic phase were divided into the control group and groups A,B and C. The control group was only added with medium. Group A was added with0. 625 μmol / L 17-AAG,group B was added with 1. 0 μg / m L DDP,and group C was added with 0. 625 μg / m L 17-AAG and 1. 0 μg / m L DDP. After being cultured for 24 h and 48 h,the cell proliferation inhibition rates of groups A,B and C were determined by MTT,the apoptosis rate was measured by flow cytometry,and the Bax and Bcl-2 mRNA in each group was measured by RT-PCR. Results The cell proliferation inhibition rates of groups A,B and C which were cultured for 48 h were all higher than those of being cultured for 24 h( all P 0. 05),the cell proliferation inhibition rate of group C was higher than those of groups A and B at the same time of culture( all P 0. 05). After being cultured for 48 h,the apoptosis rate and Bax mRNA in the groups A,B and C were higher than that of the control group,while Bcl-2 mRNA was lower than that of the control group( all P 0. 05); the apoptosis rate and Bax mRNA of group C were higher than those of groups A and B,but the Bcl-2 mRNA was lower than those of groups A and B( all P 0. 05). Conclusions 17-AAG inhibits the growth of human hepatocellular carcinoma Hep G2 cells and has synergistic effect with cisplatin. The mechanism may be related to the up-regulation of Bax mRNA and down-regulation of Bcl-2 mRNA expression.

Key concepts: Apoptosis, Cisplatin, Molecular biology, Flow cytometry, Cell growth, Messenger RNA, Cell culture, Biology

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