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首页> 外文期刊>Integrative cancer therapies >Apoptotic effects of Physalis minima L. chloroform extract in human breast carcinoma T-47D cells mediated by c-myc-, p53-, and caspase-3-dependent pathways.
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Apoptotic effects of Physalis minima L. chloroform extract in human breast carcinoma T-47D cells mediated by c-myc-, p53-, and caspase-3-dependent pathways.

机译:酸浆氯仿提取物在依赖c-myc-,p53-和caspase-3依赖性途径介导的人乳腺癌T-47D细胞中的凋亡作用。

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摘要

The chloroform extract of Physalis minima produced a significant growth inhibition against human T-47D breast carcinoma cells as compared with other extracts with an EC(50) value of 3.8 microg/mL. An analysis of cell death mechanisms indicated that the extract elicited an apoptotic cell death. mRNA expression analysis revealed the coregulation of apoptotic genes, that is, c-myc , p53, and caspase-3. The c-myc was significantly induced by the chloroform extract at the earlier phase of treatment, followed by p53 and caspase-3. Biochemical assay and ultrastructural observation displayed typical apoptotic features in the treated cells, including DNA fragmentation, blebbing and convolution of cell membrane, clumping and margination of chromatin, and production of membrane-bound apoptotic bodies. The presence of different stages of apoptotic cell death and phosphatidylserine externalization were further reconfirmed by annexin V and propidium iodide staining. Thus, the results from this study strongly suggest that the chloroform extract of P. minima induced apoptotic cell death via p53-, caspase-3-, and c-myc-dependent pathways.
机译:与其他具有EC(50)值3.8 microg / mL的提取物相比,酸浆的氯仿提取物对人T-47D乳腺癌细胞产生了显着的生长抑制作用。对细胞死亡机制的分析表明,该提取物引起凋亡性细胞死亡。 mRNA表达分析揭示了凋亡基因,即c-myc,p53和caspase-3的共调节。在治疗的早期阶段,氯仿提取物可明显诱导c-myc,随后是p53和caspase-3。生化分析和超微结构观察显示了处理过的细胞中典型的凋亡特征,包括DNA片段化,细胞膜起泡和卷积,染色质聚集和边缘化以及膜结合的凋亡小体的产生。膜联蛋白V和碘化丙锭染色进一步证实了凋亡细胞死亡和磷脂酰丝氨酸外在化的不同阶段的存在。因此,这项研究的结果有力地表明,最小体育杆菌的氯仿提取物通过p53-,caspase-3-和c-myc依赖性途径诱导凋亡细胞死亡。

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