Tumor necrosis factor alpha induces apoptosis of K562/VCR and K562 cells and reverses multidrug resistance
Baozhen Wang
Abstract
Baozhen Wang
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.
Key concepts: K562 cells, Apoptosis, Tumor necrosis factor alpha, Flow cytometry, Multiple drug resistance, MTT assay, Molecular biology, Cancer research