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Proliferation Inhibition and Cell Cycle Arrest of Human Hepatoma HepG-2 Cell Induced by Cinobufacini Injection

Xiaonan Cui

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Abstract

Objective To study the effect of cinobufacin injection on the proliferation and cell cycle of human hepatoma HepG-2 cell. Methods Cell proliferation was analysed by MTT assay; Flow cytometry (FCM) was emplayed to detect tumor cell cycle distribution; Expression of CyclinA, CDK2 mRNA levels in HepG-2 cells was analysed by PT-PCR;Quantitative colorimetric assay was used to analyse cyclinA/CDK2 activity in HepG-2 cells .Results Cinobufacini injection significantly inhibited HepG-2 cells proliferation in doses-and time-dependent ways;FCM analysis expressed cinobufacin injection induced cell cycle arrest at S phase ;PT-PCR assay showed cinobufacin injection down-regulated CDK2, CyclinA expression at mRNA levels; Quantitative colorimetric assay displayed cinobufacin injection deceased cyclinA/CDK2 activity in HepG-2 cells.Conclusion Human hepotocarcinoma HepG-2 cell growth can be inhibited and cell cycle can be induced to arrest at S phase through injection.Conclusion The mechanism might be partly related to the down-regulation of CDK2, CyclinA expression and inhibition of cyclinA/CDK2 activity .

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Objective To study the effect of cinobufacin injection on the proliferation and cell cycle of human hepatoma HepG-2 cell. Methods Cell proliferation was analysed by MTT assay; Flow cytometry (FCM) was emplayed to detect tumor cell cycle distribution; Expression of CyclinA, CDK2 mRNA levels in HepG-2 cells was analysed by PT-PCR;Quantitative colorimetric assay was used to analyse cyclinA/CDK2 activity in HepG-2 cells .Results Cinobufacini injection significantly inhibited HepG-2 cells proliferation in doses-and time-dependent ways;FCM analysis expressed cinobufacin injection induced cell cycle arrest at S phase ;PT-PCR assay showed cinobufacin injection down-regulated CDK2, CyclinA expression at mRNA levels; Quantitative colorimetric assay displayed cinobufacin injection deceased cyclinA/CDK2 activity in HepG-2 cells.Conclusion Human hepotocarcinoma HepG-2 cell growth can be inhibited and cell cycle can be induced to arrest at S phase through injection.Conclusion The mechanism might be partly related to the down-regulation of CDK2, CyclinA expression and inhibition of cyclinA/CDK2 activity .

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Available abstract

Objective To study the effect of cinobufacin injection on the proliferation and cell cycle of human hepatoma HepG-2 cell. Methods Cell proliferation was analysed by MTT assay; Flow cytometry (FCM) was emplayed to detect tumor cell cycle distribution; Expression of CyclinA, CDK2 mRNA levels in HepG-2 cells was analysed by PT-PCR;Quantitative colorimetric assay was used to analyse cyclinA/CDK2 activity in HepG-2 cells .Results Cinobufacini injection significantly inhibited HepG-2 cells proliferation in doses-and time-dependent ways;FCM analysis expressed cinobufacin injection induced cell cycle arrest at S phase ;PT-PCR assay showed cinobufacin injection down-regulated CDK2, CyclinA expression at mRNA levels; Quantitative colorimetric assay displayed cinobufacin injection deceased cyclinA/CDK2 activity in HepG-2 cells.Conclusion Human hepotocarcinoma HepG-2 cell growth can be inhibited and cell cycle can be induced to arrest at S phase through injection.Conclusion The mechanism might be partly related to the down-regulation of CDK2, CyclinA expression and inhibition of cyclinA/CDK2 activity .

Key concepts: Cell cycle, Flow cytometry, Cyclin-dependent kinase 2, Cell growth, Cell cycle checkpoint, MTT assay, Cell, Cell biology

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