Different effect of protein kinase B/Akt and extracellular signal-regulated kinase inhibition on trichostatin A-induced apoptosis in epithelial ovarian carcinoma cell lines.
作者： Eun-Ra Jang , Yun Jeong Kim , Soon Chul Myung , Wonyong Kim , Chung Soo Lee
DOI: 10.1007/S11010-011-0768-7
关键词: Trichostatin A 、 MAPK/ERK pathway 、 Programmed cell death 、 Protein kinase B 、 Caspase 、 Histone deacetylase 、 Signal transduction 、 Cell biology 、 Apoptosis 、 Cancer research 、 Chemistry
摘要: Histone deacetylase inhibitor-induced apoptosis in cancer cells may be mediated by the Ras/Raf/MEK/ERK and protein kinase B/Akt signaling pathways. However, inhibition of ERK Akt activity has different effects on proliferation cells. We assessed compared inhibitory pathways apoptotic effect trichostatin A using human epithelial carcinoma cell lines OVCAR-3 SK-OV-3. Trichostatin induced nuclear damage, decrease Bid Bcl-2 levels, increase Bax cytochrome c release, activation caspases (8, 9, 3) tumor suppressor p53 levels. inhibitor potentiated A-induced apoptosis-related death, whereas exhibited an additive toxic effect. These results suggest that inhibitors have a differential ovarian lines. potentiate increasing caspase-8-dependent pathway mitochondria-mediated death pathway, leading to caspase activation. In contrast, exhibit toxicity
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