Source:http://linkedlifedata.com/resource/pubmed/id/20717005
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007137,
umls-concept:C0007600,
umls-concept:C0109317,
umls-concept:C0460004,
umls-concept:C0538927,
umls-concept:C0596290,
umls-concept:C0752312,
umls-concept:C1120843,
umls-concept:C1150579,
umls-concept:C1333340,
umls-concept:C1366882,
umls-concept:C1370600,
umls-concept:C1518174,
umls-concept:C1705767,
umls-concept:C1705791,
umls-concept:C1879547
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pubmed:issue |
9
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pubmed:dateCreated |
2010-9-2
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pubmed:abstractText |
It has been observed that several cyclooxygenase-2 (COX-2) inhibitory chemicals might inhibit proliferation of various cancer cells through COX-2-independent action. We also identified that celecoxib more selectively kills cell lines derived from head and neck squamous cell carcinoma (HNSCC) than its non-cancerous counterparts, irrespective of COX-2 expression. Herein, we investigated whether the regulation of mitogen-activated protein kinases activity might be one of the main mechanisms related to a conspicuous COX-2-independent tumor-killing effect of celecoxib in HNSCC cell lines. We assessed the effect of celecoxib on extracellular signal-regulated kinase (ERK), p38, and c-Jun NH2-terminal kinase activity by a transcription factor activation assay then evaluated, if these factors might be involved in the COX-2-independent tumor-killing effect of celecoxib by blocking their activity. We found that the blocking activation of ERK and/or p38 could reverse the celecoxib-induced cell growth inhibition by 50-80% in HNSCC cell lines, but it was not tested in cancer cells of other types. In conclusion, our study suggests that most COX-2-independent tumor-killing action of celecoxib is mediated by the upregulation of ERK and/or p38 activity in HNSCC cells. These results encourage investigation on the underlying mechanisms and detailed outcomes of mitogen-activated protein kinases activation by celecoxib more concisely, for using its excellent tumor-killing effect more safely in the clinical field of cancer treatment.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antineoplastic Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2 Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/JNK Mitogen-Activated Protein...,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides,
http://linkedlifedata.com/resource/pubmed/chemical/celecoxib,
http://linkedlifedata.com/resource/pubmed/chemical/p38 Mitogen-Activated Protein...
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1473-5741
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
823-30
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pubmed:meshHeading |
pubmed-meshheading:20717005-Antineoplastic Agents,
pubmed-meshheading:20717005-Carcinoma, Squamous Cell,
pubmed-meshheading:20717005-Cell Line, Tumor,
pubmed-meshheading:20717005-Cell Proliferation,
pubmed-meshheading:20717005-Cyclooxygenase 2 Inhibitors,
pubmed-meshheading:20717005-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:20717005-Head and Neck Neoplasms,
pubmed-meshheading:20717005-Humans,
pubmed-meshheading:20717005-JNK Mitogen-Activated Protein Kinases,
pubmed-meshheading:20717005-Pyrazoles,
pubmed-meshheading:20717005-Sulfonamides,
pubmed-meshheading:20717005-Up-Regulation,
pubmed-meshheading:20717005-p38 Mitogen-Activated Protein Kinases
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pubmed:year |
2010
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pubmed:articleTitle |
Celecoxib inhibits cell proliferation through the activation of ERK and p38 MAPK in head and neck squamous cell carcinoma cell lines.
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pubmed:affiliation |
Cancer Research Institute, Seoul National University College of Medicine, Seoul National University Medical Research Center, Seoul National University Hospital, Seoul, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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