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紫杉醇诱导人肝癌QGY-7703细胞系中Bcl-2蛋白磷酸化。

Taxol induced Bcl-2 protein phosphorylation in human hepatocellular carcinoma QGY-7703 cell line.

作者信息

Cheng S C, Luo D, Xie Y

机构信息

Department of Biology, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, SAR China.

出版信息

Cell Biol Int. 2001;25(3):261-5. doi: 10.1006/cbir.2000.0619.

Abstract

Bcl-2 family proteins play a critical role in the regulation of apoptosis. Treatment of a human hepatocellular carcinoma cell line, QGY-7703, with Taxol induced apoptosis and Bcl-2 protein phosphorylation. Microscopic observation indicated that apoptotic bodies (0-15%) of Taxol-treated QGY cells appeared after 12 h of treatment, and apoptotic QGY cells gradually increased to 40% after 24 h and 70% after 48 h. A DNA fragmentation assay showed that Taxol induced genomic DNA cleavage into 200 bp DNA fragments. Bcl-2 protein was phosphorylated in Taxol-treated QGY cells within 3 h of treatment, and continued gradually up to 24 h. By 48 h, the protein was unphosphorylated. Other Bcl-2 family proteins, including Bax (a heterodimerization partner of Bcl-2), Bcl-XL, Bak and Bad, were expressed, but at constant levels. The results show a close correlation between Bcl-2 phosphorylation and apoptosis in QGY cells. The inactivation of Bcl-2 protein phosphorylation could be one of the key mechanisms needed for the induction of apoptosis in Taxol-treated QGY cells.

摘要

Bcl-2家族蛋白在细胞凋亡调控中发挥关键作用。用紫杉醇处理人肝癌细胞系QGY-7703可诱导细胞凋亡和Bcl-2蛋白磷酸化。显微镜观察表明,紫杉醇处理的QGY细胞在处理12小时后出现凋亡小体(0 - 15%),24小时后凋亡的QGY细胞逐渐增加到40%,48小时后增加到70%。DNA片段化分析表明,紫杉醇诱导基因组DNA裂解为200 bp的DNA片段。在紫杉醇处理的QGY细胞中,Bcl-2蛋白在处理3小时内发生磷酸化,并持续逐渐增加直至24小时。到48小时时,该蛋白去磷酸化。其他Bcl-2家族蛋白,包括Bax(Bcl-2的异二聚化伙伴)、Bcl-XL、Bak和Bad均有表达,但水平恒定。结果表明QGY细胞中Bcl-2磷酸化与细胞凋亡密切相关。Bcl-2蛋白磷酸化失活可能是紫杉醇处理的QGY细胞诱导凋亡所需的关键机制之一。

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