2013Zhongguo yaolixue tongbaoRequires access

Relations of Cadmium(II) complex of pyrazolone derivatives induced apoptosis with Bax and Bcl-2 in esophageal cancer cells

Wu Tin

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Abstract

Aim To investigate the appotosis induced by Cadmium(Ⅱ) complex of pyrazolone derivatives(Ls-17) and its effect on the expression of Bax and Bcl-2 protein in the esophageal cancer cells(Eca109).Methods After the treatment of Eca-109 cells with Ls-17,cell viability was detected by MTT assay;cell apoptosis and cell cycle profile were tested by flow cytometry assay;the activity of caspase-3 and 9 were tested using Caspase Activity Assay Kit,and Bax and Bcl-2 expression levels were detected by Western blot.Results Ls-17 significantly inhibited the proliferation of Eca-109 cells with an IC 50 value 25.12 mg·L-1.It also induced Eca-109 cell apoptosis(P 0.01),and cell cycle arrest in G 2 / M phase.Ls-17 significantly reduced mitochondria membrane potential and enhanced caspase-3 and 9 activities,as well as increased Bax / Bcl-2 ratio.Conclusion Ls-17 can effectively inhibit the proliferation of Eca-109 cells by induction of apoptosis.The molecular mechanism may be related with down-regulation of Bcl-2 and up-regulation of Bax / Bcl2 ratio.

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Aim To investigate the appotosis induced by Cadmium(Ⅱ) complex of pyrazolone derivatives(Ls-17) and its effect on the expression of Bax and Bcl-2 protein in the esophageal cancer cells(Eca109).Methods After the treatment of Eca-109 cells with Ls-17,cell viability was detected by MTT assay;cell apoptosis and cell cycle profile were tested by flow cytometry assay;the activity of caspase-3 and 9 were tested using Caspase Activity Assay Kit,and Bax and Bcl-2 expression levels were detected by Western blot.Results Ls-17 significantly inhibited the proliferation of Eca-109 cells with an IC 50 value 25.12 mg·L-1.It also induced Eca-109 cell apoptosis(P 0.01),and cell cycle arrest in G 2 / M phase.Ls-17 significantly reduced mitochondria membrane potential and enhanced caspase-3 and 9 activities,as well as increased Bax / Bcl-2 ratio.Conclusion Ls-17 can effectively inhibit the proliferation of Eca-109 cells by induction of apoptosis.The molecular mechanism may be related with down-regulation of Bcl-2 and up-regulation of Bax / Bcl2 ratio.

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Available abstract

Aim To investigate the appotosis induced by Cadmium(Ⅱ) complex of pyrazolone derivatives(Ls-17) and its effect on the expression of Bax and Bcl-2 protein in the esophageal cancer cells(Eca109).Methods After the treatment of Eca-109 cells with Ls-17,cell viability was detected by MTT assay;cell apoptosis and cell cycle profile were tested by flow cytometry assay;the activity of caspase-3 and 9 were tested using Caspase Activity Assay Kit,and Bax and Bcl-2 expression levels were detected by Western blot.Results Ls-17 significantly inhibited the proliferation of Eca-109 cells with an IC 50 value 25.12 mg·L-1.It also induced Eca-109 cell apoptosis(P 0.01),and cell cycle arrest in G 2 / M phase.Ls-17 significantly reduced mitochondria membrane potential and enhanced caspase-3 and 9 activities,as well as increased Bax / Bcl-2 ratio.Conclusion Ls-17 can effectively inhibit the proliferation of Eca-109 cells by induction of apoptosis.The molecular mechanism may be related with down-regulation of Bcl-2 and up-regulation of Bax / Bcl2 ratio.

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

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