期刊
CANCER LETTERS
卷 331, 期 2, 页码 183-191出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2012.12.020
关键词
ASC; DLD-1; Methylation; DNA damaging agent; Cell death
类别
资金
- National R&D Program for Cancer Control, Ministry for Health, Welfare and Family affairs, Korea [1020190]
- Basic Science Research Program through NRF
- MEST [2010-10849]
- NIH [AG14357, AR055398]
- Korea Health Promotion Institute [1020190] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), an essential component of the inflammasome complex, is frequently silenced by epigenetic methylation in many tumor cells. Here, we demonstrate that restoration of ASC expression in human colorectal cancer DLD-1 cells, in which ASC is silenced by aberrant methylation, potentiated cell death mediated by DNA damaging agent. Contrarily, ASC knockdown in HT-29 cells rendered cells less susceptible to etoposide toxicity. The increased susceptibility of ASC-expressing DLD-1 cells to genotoxic stress was independent of inflammasome or caspase activation, but partially dependent on mitochondrial ROS production and JNK activation. Thus, our data suggest that ASC expression in cancer cells is an important factor in determining their susceptibility to chemotherapy. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
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