Linked Life Data

17097066

Source:http://linkedlifedata.com/resource/pubmed/id/17097066

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pubmed-article:17097066pubmed:abstractTextWe established TRAIL-resistant MDA-231/TR cells from MDA-231 parent cells to understand the mechanism of TRAIL resistance in breast cancer cells. The selected TRAIL-resistant cells were cross-resistant to TNF-alpha/cycloheximide but remained sensitive to DNA-damage drugs such as oxaliplatin and etoposide. The expression levels of death receptors (DR4 and DR5), FADD, cIAP1, cIAP2, and Bcl-2 family were not changed in TRAIL-treated both cells. Significant down-regulation of XIAP and cFLIP was occurred after TRAIL treatment in MDA-231 cells whereas their levels were sustained in MDA-231/TR cells. TRAIL-mediated activation of ERK and JNK were also observed in parent MDA-231 cells but not in MDA-231/TR cells. However, TRAIL-resistant cells showed constitutive activation state after treatment with TRAIL. Pretreatment with PD98059 or transfection of MKK1-DN (dominant negative) expression vector attenuated TRAIL resistance in MDA-231/TR cells. Our findings provide the evidence that the sustained expression level of cFLIP(L) and XIAP protein and constitutive ERK activation may lead to acquired TRAIL resistance in breast cancer cells.lld:pubmed
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pubmed-article:17097066pubmed:dateRevised2009-11-19lld:pubmed
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pubmed-article:17097066pubmed:articleTitleAcquired TRAIL resistance in human breast cancer cells are caused by the sustained cFLIP(L) and XIAP protein levels and ERK activation.lld:pubmed
pubmed-article:17097066pubmed:affiliationDepartment of Immunology, School of Medicine, Keimyung University, 194 DongSan-Dong Jung-Gu, Taegu 700-712, Republic of Korea.lld:pubmed
pubmed-article:17097066pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:17097066pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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