2004Shiyong zhongliu zazhiRequires access

Tumor necrosis factor alpha induces apoptosis of K562/VCR and K562 cells and reverses multidrug resistance

Baozhen Wang

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Abstract

Objective To study the mechanism of apoptosis and reverse of multidrug resistance induced by tumor necrosis factor alpha(TNFα) in K562/VCR and K562 cells in vitro.Methods Apoptosis was observed by optic and electron microscopes and flow cytometry.P-gp and bcl-2 expression was assayed by flow cytometry.Drug chemosensitivity was analyzed by MTT.Results Apoptosis was more significant in K562/VCR cells than in K562 cells after exposured to 100 U/ml TNFα for 48 hours.After treatment with 1 000 U/ml TNFα,apoptosis rates of K562/VCR and K562 cells were 29.4% and 10.7%,respectively.After treatment with 1 000 U/ml TNFα for 72 hours,expression of P-gp decreased from 93.6% to 82.4%,and expression of bcl-2 from 32.9% to 7.0%.After treatment with TNFα,chemosensitivities of K562/VCR and K562 cells to VCR,Ara-C and VP-16 were increased (P0.05).Conclusion TNFα can induce apoptosis both for K562 and K562/VCR cells;the mechanisum for TNFα to reverse MDR of K562/VCR may involve the downregulation of bcl-2 expression.

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Objective To study the mechanism of apoptosis and reverse of multidrug resistance induced by tumor necrosis factor alpha(TNFα) in K562/VCR and K562 cells in vitro.Methods Apoptosis was observed by optic and electron microscopes and flow cytometry.P-gp and bcl-2 expression was assayed by flow cytometry.Drug chemosensitivity was analyzed by MTT.Results Apoptosis was more significant in K562/VCR cells than in K562 cells after exposured to 100 U/ml TNFα for 48 hours.After treatment with 1 000 U/ml TNFα,apoptosis rates of K562/VCR and K562 cells were 29.4% and 10.7%,respectively.After treatment with 1 000 U/ml TNFα for 72 hours,expression of P-gp decreased from 93.6% to 82.4%,and expression of bcl-2 from 32.9% to 7.0%.After treatment with TNFα,chemosensitivities of K562/VCR and K562 cells to VCR,Ara-C and VP-16 were increased (P0.05).Conclusion TNFα can induce apoptosis both for K562 and K562/VCR cells;the mechanisum for TNFα to reverse MDR of K562/VCR may involve the downregulation of bcl-2 expression.

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Available abstract

Objective To study the mechanism of apoptosis and reverse of multidrug resistance induced by tumor necrosis factor alpha(TNFα) in K562/VCR and K562 cells in vitro.Methods Apoptosis was observed by optic and electron microscopes and flow cytometry.P-gp and bcl-2 expression was assayed by flow cytometry.Drug chemosensitivity was analyzed by MTT.Results Apoptosis was more significant in K562/VCR cells than in K562 cells after exposured to 100 U/ml TNFα for 48 hours.After treatment with 1 000 U/ml TNFα,apoptosis rates of K562/VCR and K562 cells were 29.4% and 10.7%,respectively.After treatment with 1 000 U/ml TNFα for 72 hours,expression of P-gp decreased from 93.6% to 82.4%,and expression of bcl-2 from 32.9% to 7.0%.After treatment with TNFα,chemosensitivities of K562/VCR and K562 cells to VCR,Ara-C and VP-16 were increased (P0.05).Conclusion TNFα can induce apoptosis both for K562 and K562/VCR cells;the mechanisum for TNFα to reverse MDR of K562/VCR may involve the downregulation of bcl-2 expression.

Key concepts: K562 cells, Apoptosis, Tumor necrosis factor alpha, Flow cytometry, Multiple drug resistance, MTT assay, Molecular biology, Cancer research

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