Epigallocatechin-3-Gallate Triggers Mitochondrial-Mediated Apoptosis and Suppresses EGFR Signaling in Cervical Cancer Cells

Abstract

Background: Cervical cancer is associated with a relatively high mortality rate in women. Conventional therapies often cause significant adverse effects, highlighting the need for novel treatments with improved safety and efficacy. Objectives: Considering that epigallocatechin-3-gallate (EGCG) has anticancer effects in various malignancies, this study evaluated the impacts of EGCG on cervical cancer cells, with emphasis on identifying the mechanism of action. Methods: After culture, HeLa and CaSki cells were exposed to a range of EGCG concentrations. The MTT assay was used to assess cell viability, and flow cytometry was used for apoptosis. Finally, using designed primers, expression levels of bax, CASP3, p53, bcl-2, CASP9, and EGFR were quantified by qRT-PCR. Results: The EGCG decreased cell viability in both cervical cancer cell lines and increased apoptosis. Notably, at 40 and 80 μg/mL, EGCG upregulated pro-apoptotic genes (bax, p53, CASP3, CASP9) and downregulated anti-apoptotic bcl-2 and EGFR expression. Conclusions: Our findings indicate that EGCG exerts anticancer activity against cervical cancer cell lines, at least in part, by activating the intrinsic mitochondrial apoptosis pathway as well as inhibiting proliferative signaling. Further mechanistic research is needed to determine the full spectrum of EGCG’s actions in cervical cancer.