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Restoration of ASC expression sensitizes colorectal cancer cells to genotoxic stress-induced caspase-independent cell death

Authors
 Sujeong Hong  ;  Inhwa Hwang  ;  Yun-Sun Lee  ;  Sangjun Park  ;  Won-Keun Lee  ;  Teresa Fernandes-Alnemri  ;  Emad S. Alnemri  ;  You-Sun Kim  ;  Je-Wook Yu 
Citation
 CANCER LETTERS, Vol.331(2) : 183-191, 2013 
Journal Title
CANCER LETTERS
ISSN
 0304-3835 
Issue Date
2013
MeSH
Apoptosis/drug effects* ; Base Sequence ; CARD Signaling Adaptor Proteins ; Caspases/metabolism* ; Cell Line, Tumor ; Colorectal Neoplasms/enzymology ; Colorectal Neoplasms/pathology* ; Cytoskeletal Proteins/metabolism* ; DNA Methylation ; DNA Primers ; Etoposide/pharmacology ; Fluorescent Antibody Technique ; HT29 Cells ; Humans ; Inflammasomes/metabolism ; MAP Kinase Signaling System ; Mitochondria/drug effects ; Mitochondria/enzymology ; Mitochondria/metabolism ; Mutagens/toxicity* ; Reactive Oxygen Species/metabolism ; Reverse Transcriptase Polymerase Chain Reaction
Keywords
ASC ; DLD-1 ; Methylation ; DNA damaging agent ; Cell death
Abstract
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.
Files in This Item:
T201300427.pdf Download
DOI
10.1016/j.canlet.2012.12.020
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Microbiology (미생물학교실) > 1. Journal Papers
Yonsei Authors
Yu, Je Wook(유제욱) ORCID logo https://orcid.org/0000-0001-5943-4071
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/86421
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