Epidermal growth factor stimulates the proliferation of human esophageal squamous cell carcinoma HKESC-1 cells by increasing COX-2 expression.
- Author:
Le YU
1
;
Chi-hin CHO
;
Shu-wen LIU
Author Information
- Publication Type:Journal Article
- MeSH: Carcinoma, Squamous Cell; pathology; Cell Line, Tumor; Cell Proliferation; drug effects; Cyclooxygenase 2; metabolism; Dinoprostone; metabolism; Epidermal Growth Factor; pharmacology; Esophageal Neoplasms; pathology; Humans; Pyrazoles; pharmacology; Receptors, Prostaglandin E, EP2 Subtype; metabolism; Sulfonamides; pharmacology; Up-Regulation; drug effects
- From: Journal of Southern Medical University 2011;31(8):1323-1326
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanisms responsible for epidermal growth factor (EGF)-induced proliferation of human esophageal squamous cell carcinoma cells.
METHODS(3)H-thymidine incorporation assay was used to assess the proliferation of HKESC-1 cells exposed to EGF stimulation. Enzyme immunoassay was used to measure PGE(2) release from HKESC-1 cells, and the protein levels of cyclooxygenase 1 (COX-1), COX-2, EP1 and EP2 in EGF-stimulated cells were determined by Western blotting.
RESULTSEGF upregulated COX-2 protein expression but produced no obvious effect on COX-1 protein expression in HKESC-1 cells. As a consequence of increased COX-2, EGF further enhanced cellular PGE(2) release. EGF stimulation also resulted in increased protein expression of EP2, a subtype of PGE(2) receptors. Both the non-selective COX inhibitor indomethacin and the selective COX-2 inhibitor SC-236 completely abolished EGF-induced PGE(2) release, and suppressed the mitogenic effect of EGF.
CONCLUSIONEGF stimulates the proliferation of HKESC-1 cells by increasing COX-2 protein expression and PGE(2) release. Upregulated EP2 protein expression may further amplify the mitogenic action of PGE(2).
