102 372

Cited 12 times in

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

Authors
Hong, S; Hwang, I; Lee, YS; Park, S; Lee, WK; Fernandes-Alnemri, T; Alnemri, ES; Kim, YS; Yu, JW
Citation
Cancer letters, 331(2):183-191, 2013
Journal Title
Cancer letters
ISSN
0304-38351872-7980
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.
MeSH terms
Apoptosis/*drug effectsBase SequenceCaspases/*metabolismCell Line, TumorColorectal Neoplasms/enzymology/*pathologyCytoskeletal Proteins/*metabolismDNA MethylationDNA PrimersEtoposide/pharmacologyFluorescent Antibody TechniqueHT29 CellsHumansInflammasomes/metabolismMAP Kinase Signaling SystemMitochondria/drug effects/enzymology/metabolismMutagens/*toxicityReactive Oxygen Species/metabolismReverse Transcriptase Polymerase Chain Reaction
DOI
10.1016/j.canlet.2012.12.020
PMID
23321501
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
AJOU Authors
김, 유선
Full Text Link
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML

qrcode

해당 아이템을 이메일로 공유하기 원하시면 인증을 거치시기 바랍니다.

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

Browse