Journal
ONCOLOGY REPORTS
Volume 38, Issue 4, Pages 2489-2497Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2017.5921
Keywords
chaetocin; intrahepatic cholangiocarcinoma; cell viability; apoptosis; reactive oxygen species; cell cycle; ASK-1; JNKs
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Funding
- Natural Science Foundation of China [81641110]
- Guangdong Province Natural Science Foundation [2015A030313725]
- Guangdong Science Province and Technology Program projects [2012B031800411]
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The present study demonstrated that chaetocin, a natural small-molecule product produced by Chaetomium fungal species and a potential anticancer agent, inhibited the viability and invasive ability of the human intrahepatic cholangio-carcinoma cell line CCLP-1 in vivo and in vitro as revealed by CCK-8 and Transwell invasion assays and mouse xenograft tumor experiments. As determined using flow cytometry and intracellular ROS assays, chaetocin was found to induce cell cycle arrest and oxidative stress, leading to CCLP-1 cell apoptosis. Cell apoptosis can be initiated via different apoptotic signaling pathways under oxidative stress. As determined by western blot analysis, expression levels of the apoptosis signal-regulating kinase 1 (ASK-1) signalosome and its downstream c-Jun N-terminal kinase (JNK) signaling pathway were increased under oxidative stress stimulation. These findings indicate that chaetocin arrests the cell cycle and induces apoptosis by regulating the reactive oxygen species-mediated ASK-1/JNK signaling pathways.
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