[Epidermal growth factor stimulates the proliferation of human esophageal squamous cell carcinoma HKESC-1 cells by increasing COX-2 expression]
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Updated: May 29, 2026

Modeling Oral-Esophageal Squamous Cell Carcinoma in 3D Organoids
Published on: December 23, 2022
Le Yu1, Chi-hin Cho, Shu-wen Liu
1School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, China. yule0423@gmail.com
Objective:
To 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.
Results:
EGF 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.
Conclusion:
EGF 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).
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