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Archive > Volume 23 Issue 3 > 2016,23(3):350-354. DOI:10.3872/j.issn.1007-385X.2016.03.009 Prev Next
Basic Research
Platycodin D induced apoptosis of breast cancer MDA-MB-231 cell
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Abstract:
Objective:This study was designed to estimate the role of platycodin D (PD), a natural monomeric compound derived from platycodin grandiflorum, in apoptosis of highly metastatic breast cancer cell line MDA-MB-231 and to primarily explore the possible mechanisms. Methods: MDA-MB-231 cells were treated with different concentrations of PD (0, 2.5, 5, 10 μmol/L), cell proliferation rate was detected by MTT and IC50 value was calculated; cell apoptosis was evaluated by Flow cytometry, and the expressions of apoptosis-related proteins were assessed by Western blotting. Results: PD significantly inhibited MDA-MB-231 cell proliferation (P＜0.01) in a dose-dependent manner with a IC50 value of (7.30±2.67) μmol/L at 72 h. Compared with control group, 10 μmol/L PD could significantly promote the apoptosis of MDA-MB-231 cells (P<0.05). PD increased the caspase protein activity by up-regulating active cleaved caspase-3, -8 and -9 and down-regulating inactive caspase-8 and -9. PD also decreased the expression level of Bcl-2 and increased Bax expression, resulting in the decrease of Bcl-2/Bax ratio in MDA-MB-231 cells. The protein expression of mutant P53 was down-regulated after treated with PD; otherwise, the expression of E2F1 was up-regulated. Conclusion：PD had an obvious anticancer effect by inhibiting breast cancer cell proliferation, and inducing apoptosis might be a potential mechanism of anti-cancer effects.
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Project Supported:
Projects supported by the National Natural Science Foundation of China（No. 81171991）
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