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c‐Jun N‐terminal kinase negatively regulates epidermal growth factor‐induced cyclooxygenase‐2 expression in oral squamous cell carcinoma cell lines
Author(s) -
Husvik Camilla,
Bryne Magne,
Halstensen Trond S.
Publication year - 2009
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/j.1600-0722.2009.00682.x
Subject(s) - epidermal growth factor , kinase , p38 mitogen activated protein kinases , transcription factor , cancer research , microbiology and biotechnology , c jun , biology , signal transduction , chemistry , protein kinase a , cell culture , biochemistry , genetics , gene
Epidermal growth factor (EGF)‐induced cyclooxygenase‐2 (COX‐2) expression in squamous cell carcinomas is mediated through the extracellular signal‐regulated kinase 1/2 and p38 pathways. Examination of a basaloid and a conventional oral squamous cell carcinoma cell line revealed that inhibition of c‐Jun N‐terminal kinase (JNK) with SP600125 increased EGF‐induced (but not basal) COX‐2 transcription 1.5–1.9‐fold in extracellular signal‐regulated kinase 1/2 and p38 pathway‐dependent manners. Although JNK may phosphorylate the cyclosporine A‐sensitive transcription factor, nuclear factor of activated T cells c3, it was seemingly not involved because cyclosporine A did not reduce EGF‐induced COX‐2 expression. Thus, JNK negatively regulated EGF‐induced extracellular signal‐regulated kinase 1/2 and/or p38‐mediated COX‐2 transcription, presumably through activating an unidentified phosphatase.