|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0109317,
umls-concept:C0385242,
umls-concept:C0439661,
umls-concept:C0441889,
umls-concept:C0528561,
umls-concept:C0683598,
umls-concept:C0752312,
umls-concept:C1150579,
umls-concept:C1314792,
umls-concept:C1333340,
umls-concept:C1336646,
umls-concept:C1366882,
umls-concept:C1370600,
umls-concept:C1512505,
umls-concept:C1705767,
umls-concept:C1705791,
umls-concept:C1879547
|
|
pubmed:issue |
4
|
|
pubmed:dateCreated |
2006-11-19
|
|
pubmed:abstractText |
We 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.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Dec
|
|
pubmed:issn |
0006-291X
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
29
|
|
pubmed:volume |
351
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
1024-30
|
|
pubmed:dateRevised |
2009-11-19
|
|
pubmed:meshHeading |
pubmed-meshheading:17097066-Breast Neoplasms,
pubmed-meshheading:17097066-CASP8 and FADD-Like Apoptosis Regulating Protein,
pubmed-meshheading:17097066-Caspase 8,
pubmed-meshheading:17097066-Down-Regulation,
pubmed-meshheading:17097066-Drug Resistance, Neoplasm,
pubmed-meshheading:17097066-Enzyme Activation,
pubmed-meshheading:17097066-Flavonoids,
pubmed-meshheading:17097066-Humans,
pubmed-meshheading:17097066-Mitogen-Activated Protein Kinases,
pubmed-meshheading:17097066-Protein Kinase Inhibitors,
pubmed-meshheading:17097066-TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:17097066-Tumor Cells, Cultured,
pubmed-meshheading:17097066-X-Linked Inhibitor of Apoptosis Protein
|
|
pubmed:year |
2006
|
|
pubmed:articleTitle |
Acquired TRAIL resistance in human breast cancer cells are caused by the sustained cFLIP(L) and XIAP protein levels and ERK activation.
|
|
pubmed:affiliation |
Department of Immunology, School of Medicine, Keimyung University, 194 DongSan-Dong Jung-Gu, Taegu 700-712, Republic of Korea.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
