Chloramphenicol-induced mitochondrial stress increases p21 expression and prevents cell apoptosis through a p21-dependent pathway

Ching Hao Li, Su Liang Tzeng, Yu Wen Cheng, Jaw Jou Kang

研究成果: 雜誌貢獻文章同行評審

47 引文 斯高帕斯(Scopus)

摘要

Pretreatment of HepG2 and H1299 cells with chloramphenicol rendered the cells resistant to mitomycin-induced apoptosis. Both mitomycin-induced caspase 3 activity and PARP activation were also inhibited. The mitochondrial DNA-encoded Cox I protein, but not nuclear-encoded proteins, was down-regulated in chloramphenicol-treated cells. Cellular levels of the p21waf1/cip1 protein and p21waf1/cip1 mRNA were increased through a p53-independent pathway, possibly because of the stabilization of p21 waf1/cip1 mRNA in chloramphenicol-treated cells. The p21 waf1/cip1 was redistributed from the perinuclear region to the cytoplasm and co-localized with mitochondrial marker protein. Several morphological changes and activation of the senescence-associated biomarker, SA β-galactosidase, were observed in these cells. Both p21waf1/cip1 antisense and small interfering RNA could restore apoptotic-associated caspase 3 activity, PARP activation, and sensitivity to mitomycin-induced apoptosis. Similar effects were seen with other antibiotics that inhibit mitochondrial translation, including minocycline, doxycycline, and clindamycin. These findings suggested that mitochondrial stress causes resistance to apoptosis through a p21-dependent pathway.
原文英語
頁(從 - 到)26193-26199
頁數7
期刊Journal of Biological Chemistry
280
發行號28
DOIs
出版狀態已發佈 - 七月 15 2005
對外發佈

ASJC Scopus subject areas

  • 生物化學
  • 分子生物學
  • 細胞生物學

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