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[Objectives] To investigate the mechanism of DNA damage of cisplatin( DDP),a broad spectrum anticancer drug on breast cancer MCF-7 cells,and to study the mechanism of apoptosis induced by DDP.[Methods]MCF-7 cells were treated by DDP( 0 mg/L,2 mg/L,4 mg/L,6 mg/L,6 mg/L,and 10 mg/L) for 48 hours. MTT assay was used to detect the inhibitory effect of DDP on MCF-7 cells and IC50 value was calculated. Western blot was adopted to detect the expression of γ-H2 AX,which was the marker of DNA double stranded breaks( DSBs) and ATM( sensory molecules of DSBs),the apoptotic signal transduction molecule cleaved caspase-3,and the proteins associated with apoptosis calpain.[Results]DDP inhibited MCF-7 cell activity in a concentration-dependent manner and IC50 was 7. 57 mg/L. In contrast to the control group( without DDP treatment),MCF-7 cells with DDP treatment expressed more γ-H2 AX,ATM,cleaved caspase-3 and calpain.[Conclusions] DDP could inhibit the activity of breast cancer MCF-7 cells. Its mechanisms may be associated with inhibition of MCF-7 cell apoptosis,induction of DNA double strand breaking and the expression of pro-apoptotic protein up-regulation.
To investigate the mechanism of DNA damage of cisplatin (DDP), a broad spectrum anticancer drug on breast cancer MCF-7 cells, and to study the mechanism of apoptosis induced by DDP. [Methods] MCF-7 cells were treated by DDP (0 mg / L, 2 mg / L, 4 mg / L, 6 mg / L, 6 mg / L, and 10 mg / L) for 48 hours. MTT assay was used to detect the inhibitory effect of DDP on MCF -7 cells and IC50 value was calculated. Western blot was adopted to detect the expression of γ-H2 AX, which was the marker of DNA double stranded breaks (DSBs) and ATM (sensory molecules of DSBs), the apoptotic signal transduction molecule cleaved caspase-3, and the proteins associated with apoptosis calpain. [Results] DDP inhibited MCF-7 cell activity in a concentration-dependent manner and IC50 was 7. 57 mg / L. In contrast to the control group (without DDP treatment), [Conclusions] DDP could inhibit the activity of breast cancer MCF-7 cells. Its mec hanisms may be associated with inhibition of MCF-7 cell apoptosis, induction of DNA double strand breaking and the expression of pro-apoptotic protein up-regulation.