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首页> 外文期刊>International journal of molecular medicine >Curcumin inhibits proliferation and migration by increasing the Bax to Bcl-2 ratio and decreasing NF-kappaBp65 expression in breast cancer MDA-MB-231 cells.
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Curcumin inhibits proliferation and migration by increasing the Bax to Bcl-2 ratio and decreasing NF-kappaBp65 expression in breast cancer MDA-MB-231 cells.

机译：姜黄素通过增加乳腺癌MDA-MB-231细胞中Bax与Bcl-2的比率并降低NF-κBp65表达来抑制增殖和迁移。

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摘要

Curcumin (1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione), is extracted from the plant Curcuma longa. It has cytotoxic effects and induces apoptosis in many human cancer cells but the molecular mechanisms are not fully understood. In the present study, we evaluated the effects of curcumin on human breast cancer MDA-MB-231 cells. The cytotoxic effects of curcumin on MDA-MB-231 cells were measured by MTT assay. The percentages of cell cycle were determined by flow cytometry. The protein expressions of p21, 53, Bax and Bcl-2 were examined by Western blotting. The results show that curcumin inhibits the proliferation of MDA-MB-231 cells and induces G2/M arrest in a dose-dependent manner. Curcumin increased the protein expressions of p21 and Bax, but decreased the protein expression of p53 and Bcl-2 in MDA-MB-231 cells. Our results show that one molecular mechanism of curcumin inhibits the proliferation of MDA-MB-231 cells either through up-regulating p21 expression and then inducing apoptosis,or through up-regulating the Bax to Bcl-2 ratio and then inducing apoptosis. Our results also show that curcumin inhibits the migratory activity of MDA-MB-231 cells through down-regulating the protein expression of NF-kappaBp65. Accordingly, the therapeutic potential of curcumin for breast cancer deserves further study.
机译：从植物姜黄中提取姜黄素（1,7-双（4-羟基-3-甲氧基苯基）-1,6-庚二烯-3,5-二酮）。它具有细胞毒性作用，并在许多人类癌细胞中诱导凋亡，但其分子机制尚未完全明了。在本研究中，我们评估了姜黄素对人乳腺癌MDA-MB-231细胞的作用。用MTT法测定姜黄素对MDA-MB-231细胞的细胞毒性作用。通过流式细胞术确定细胞周期的百分比。通过蛋白质印迹检查p21、53，Bax和Bcl-2的蛋白表达。结果显示姜黄素以剂量依赖性方式抑制MDA-MB-231细胞的增殖并诱导G2 / M停滞。姜黄素可增加MDA-MB-231细胞中p21和Bax的蛋白表达，但降低p53和Bcl-2的蛋白表达。我们的结果表明姜黄素的一种分子机制是通过上调p21表达然后诱导凋亡，或通过上调Bax与Bcl-2的比例然后诱导凋亡来抑制MDA-MB-231细胞的增殖。我们的结果还表明，姜黄素通过下调NF-κBp65的蛋白表达来抑制MDA-MB-231细胞的迁移活性。因此，姜黄素对乳腺癌的治疗潜力值得进一步研究。

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