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首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Chalcone inhibits the proliferation of human breast cancer cell by blocking cell cycle progression and inducing apoptosis.
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Chalcone inhibits the proliferation of human breast cancer cell by blocking cell cycle progression and inducing apoptosis.

机译:查尔酮通过阻断细胞周期进程并诱导细胞凋亡来抑制人乳腺癌细胞的增殖。

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摘要

Chalcones are discussed to represent cancer preventive food components in a human diet that is rich in fruits and vegetables. In this study, we examined chalcone (1,3-diphenyl-2-propenone) for its effect on proliferation in human breast cancer cell lines, MCF-7 and MDA-MB-231. The results showed that chalcone inhibited the proliferation of MCF-7 and MDA-MB-231 by inducing apoptosis and blocking cell cycle progression in the G2/M phase. Immunoblot assay showed that chalcone significantly decreased the expression of cyclin B1, cyclin A and Cdc2 protein, as well as increased the expression of p21 and p27 in a p53-independent manner, contributing to cell cycle arrest. An enhancement in Fas/APO-1 and its two form ligands, membrane-bound Fas ligand (mFasL) and soluble Fas ligand (sFasL), was responsible for the apoptotic effect induced by chalcone. In addition, chalcone also triggered the mitochondrial apoptotic signaling by increasing the amount of Bax and Bak and reducing the level of Bcl-2 and Bcl-X(L), and subsequently activated caspase-9 in MCF-7 and MDA-MB-231 cells. Taken together, our study suggests that the blockade of cell cycle progression and initiation of cell apoptotic system may participate in the antiproliferative activity of chalcone in human breast cancer cells.
机译:讨论了以果蔬为代表的人类饮食中的预防性食物成分,它们代表查尔酮。在这项研究中,我们检查了查尔酮(1,3-二苯基-2-丙烯酮)对人乳腺癌细胞MCF-7和MDA-MB-231增殖的影响。结果表明查尔酮通过诱导细胞凋亡和阻断G2 / M期的细胞周期进程来抑制MCF-7和MDA-MB-231的增殖。免疫印迹分析表明查尔酮显着降低了细胞周期蛋白B1,细胞周期蛋白A和Cdc2蛋白的表达,并以不依赖p53的方式增加了p21和p27的表达,有助于细胞周期停滞。 Fas / APO-1及其两种形式的配体,膜结合的Fas配体(mFasL)和可溶性Fas配体(sFasL)的增强,是由查耳酮诱导的凋亡作用。此外,查尔酮还通过增加Bax和Bak的含量并降低Bcl-2和Bcl-X(L)的水平来触发线粒体凋亡信号,并随后激活MCF-7和MDA-MB-231中的caspase-9。细胞。综上所述,我们的研究表明,细胞周期进程的阻断和细胞凋亡系统的启动可能参与查尔酮在人乳腺癌细胞中的抗增殖活性。

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