Premium
Epidermal growth factor‐induced cyclooxygenase‐2 expression in oral squamous cell carcinoma cell lines is mediated through extracellular signal‐regulated kinase 1/2 and p38 but is Src and nuclear factor‐kappa B independent
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.1600-0722.2009.00669.x
Subject(s) - kinase , basal cell , cancer research , extracellular , epidermal growth factor , proto oncogene tyrosine protein kinase src , p38 mitogen activated protein kinases , chemistry , cell , microbiology and biotechnology , cell culture , mapk/erk pathway , medicine , biology , biochemistry , genetics
The intracellular signalling cascade(s) mediating epidermal growth factor (EGF)‐induced cyclooxygenase‐2 (COX‐2) expression is poorly defined in oral carcinomas. Investigation of two different oral squamous cell carcinoma (OSCC) cell lines with high EGF‐induced COX‐2 expression revealed, however, that this expression was dependent on two mitogen‐activated protein kinase (MAPK) pathways [extracellular signal‐regulated kinase 1/2 (ERK1/2) and p38] because combined inhibition of these pathways was needed to abolish EGF‐induced COX‐2 expression. Surprisingly, inhibition of phosphoinositide‐3 kinase (PI3K) increased EGF‐induced COX‐2 expression in the basaloid OSCC cell line (C12), suggesting a PI3K‐controlled, inhibitory COX‐2‐regulating pathway. Neither the transcription factor nuclear factor‐κB (NF‐κB), nor Src, was involved in EGF‐induced COX‐2 expression. The results suggest that EGF‐induced COX‐2 expression is regulated by several pathways, and emphasizes that individual tumors use different strategies for intracellular signalling.