Involvement of store-operated calcium signaling in EGF-mediated COX-2 gene activation in cancer cells.

Abstract:

:Growing evidence shows that chronic inflammation drives the progression of colorectal cancer (CRC). Cyclooxygenase-2 (COX-2) is one of the most important inflammatory genes involved in solid tumor metastasis. Epidermal growth factor receptor (EGFR) also plays a key role in cancer cell development. We compared the expression levels of EGFR and COX-2 between tumor and normal tissues from 20 CRC patients and studied the molecular mechanism of EGFR-mediated COX-2 gene expression in cancer cells. Our results indicated that COX-2 expression was markedly increased after EGF stimulation. COX-2 promoter analysis indicated the involvement of cyclic AMP-responsive element (CRE) and nuclear factor of activated T cells/nuclear factor interleukin-6 (NFAT/NF-IL6)-binding sites in EGF-mediated signaling pathways. Furthermore, EGF-mediated COX-2 activation was prevented by 2-aminoethoxydiphenyl borate (2-APB), a store-operated Ca(2+) channel inhibitor. Transfection of siRNA against ORAI1 or STIM1, the key regulators of store-operated Ca(2+) channels, showed significant inhibitory effects on EGF-mediated COX-2 expression. In conclusion, store-operated Ca(2+) entry is involved in the activation of transcription factors (CREB/NFAT) that are responsible for delivering EGF-mediated signals to evoke inflammatory cascades and is eventually related to CRC tumorigenesis.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Wang JY,Chen BK,Wang YS,Tsai YT,Chen WC,Chang WC,Hou MF,Wu YC,Chang WC

doi

10.1016/j.cellsig.2011.08.017

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

162-9

issue

1

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(11)00263-4

journal_volume

24

pub_type

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