The attenuation of arecoline-driven metastatic behavior in ESCC cells by EGCG is associated with alterations in EGFR-AKT-P38 signaling.
Epigallocatechin Gallate Attenuates Arecoline-induced Migration and Invasion in Esophageal Squamous Cell Carcinoma Cells Associated With EGFR/AKT/P38 Signaling.
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Abstract
BACKGROUND/AIM: Arecoline, the primary alkaloid in areca nut, is a major risk factor for metastasis-associated progression in esophageal squamous cell carcinoma (ESCC). Epigallocatechin gallate (EGCG), a major polyphenol in green tea, has exhibited anti-cancer and anti-metastatic activity in multiple tumor models. However, the effects of EGCG on arecoline-induced metastatic behavior in ESCC have not been directly examined. MATERIALS AND METHODS: In this study, we examined the effects of EGCG on arecoline-induced migration and invasion in human ESCC cells. Parental CE81T/VGH cells and a highly invasive subline, CE81T-M4, were treated with arecoline, EGCG, or their combination. Cell migration and invasion were assessed using the wound-healing and transwell assays, while changes in EGFR-related signaling and epithelial-mesenchymal transition (EMT)-associated markers were analyzed by western blotting and immunofluorescence. RESULTS: Arecoline increased ESCC cell motility and invasion and activated EGFR-dependent signaling, including AKT and P38 phosphorylation, accompanied by increased expression of EMT-associated markers. EGCG suppressed these effects in both parental and invasive ESCC cells. Genetic knockdown ofreduced P38 activation and VIMENTIN expression, supporting a role for AKT upstream of P38 in regulating EMT-related responses. CONCLUSION: The attenuation of arecoline-driven metastatic behavior in ESCC cells by EGCG is associated with alterations in EGFR-AKT-P38 signaling, supporting its potential role as a dietary or adjunctive agent in areca-associated esophageal cancer.
Affiliation
Tzyh-Chyuan Hour
External References
- PubMed ID:
- 42373249
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