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Apoptosis-like cell death of human breast cancer cell line MCF-7 induced by buprenorphine hydrochloride.

机译:盐酸丁丙诺啡诱导的人乳腺癌细胞系MCF-7的凋亡样细胞死亡。

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The analgesic buprenorphine hydrochloride (Bph) induced apoptosis-like cell death in the caspase-3-deficient human breast cancer cell line, MCF-7. This apoptosis-like cell death activated key molecules in the mitochondrial apoptotic pathway: cytochrome c, caspase-9, caspase-7, and caspase-6. Bph caused the release of fluorescent protein from the mitochondria of MCF-7 cells transfected with the pDsRed2-Mito-vector in a time-dependent manner, suggesting disruption of the mitochondrial membrane. Zn(2+) as high as 2 mM did not inhibit the DNase that took part in this apoptosis. Thus, this unidentified DNase might resemble other DNases involved in apoptosis-like cell death whose activity is not inhibited by zinc ion.
机译:镇痛药丁丙诺啡盐酸盐(Bph)在caspase-3缺陷型人乳腺癌细胞MCF-7中诱导凋亡样细胞死亡。这种凋亡样细胞死亡激活了线粒体凋亡途径中的关键分子:细胞色素c,caspase-9,caspase-7和caspase-6。 Bph导致荧光蛋白从以pDsRed2-Mito-vector转染的MCF-7细胞的线粒体中以时间依赖的方式释放,提示线粒体膜被破坏。高达2 mM的Zn(2+)不会抑制DNase参与此凋亡。因此,这种未知的DNase可能与参与凋亡样细胞死亡的其他DNase相似,后者的活性不受锌离子的抑制。

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