赫拉
紫杉醇
细胞凋亡
化学
癌症研究
细胞生物学
分子生物学
内科学
生物
细胞
生物化学
医学
癌症
作者
Vilma Maldonado,José de Anda,Jorge Meléndez-Zajgla
出处
期刊:Journal of Biochemical Toxicology
[Wiley]
日期:1996-01-01
卷期号:11 (4): 183-188
被引量:12
标识
DOI:10.1002/(sici)1522-7146(1996)11:4<183::aid-jbt3>3.0.co;2-g
摘要
Exposure of HeLa cells to different concentrations of the antineoplastic drug paclitaxel resulted in a loss of cell viability that was dependent on the concentration and time of exposure to the drug. This phenomenon was associated with the appearance of nuclear morphology typical of apoptosis and DNA breakage into a "ladder" pattern of discrete fragments of nucleosomal size. The induction of cell death was dependent on the serum concentration of the culture media, repressed by pretreatment with a cAMP-dependent protein kinase (PKA) inhibitor, and enhanced by increasing the cell proliferation with previous exposure to a cAMP-analog and a protein kinase-C (PKC) inducer. The proliferative index modifies the effect of taxol on HeLa cells, probably by means of a more rapid accumulation of cells in the G2/M cycle blockage point, although a direct participation of PKA and PKC should not be excluded.
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