Epigallocatechin-3-gallate suppressed breast oncogenesis via the miR-27a/Wnt/β-catenin pathway axis

Introduction Breast cancer is a global health concern with increased chemotherapeutic side effects and escalated chemoresistance, requiring alternative therapies. Epigallocatechin-3-gallate (EGCG), a bioactive green tea polyphenol, has exhibited promising anticancer properties. Our study aimed to investigate the tumour-suppressive effect of EGCG and its mechanism in breast cancer. Method Anticancer activities, such as cell viability, migration, cell cycle progression, and apoptosis, were evaluated. To investigate the molecular mechanism, miR-27a-3p expression was compared against EGCG, a miR-27a-3p inhibitor, and a combination of EGCG with miR-27a-3p inhibitor treatments. The influence of the individual miRNA inhibitor and its combination with EGCG on cell proliferation was also evaluated to establish the anticancer activity of EGCG via miR-27a-3p modulation. The effects of the individual miRNA inhibitor, EGCG, and their combination treatments on key Wnt/β-catenin pathway markers were examined to further establish the therapeutic route of EGCG via the miR-27a/Wnt/β-catenin pathway axis. Result EGCG notably decreased cell viability and migration, induced apoptosis, and initiated G0/G1 cell cycle arrest. Therapeutic investigation of EGCG on MDA-MB-231 cells indicated its regulatory role on oncogenic miR-27a-3p, which was confirmed when miR-27a-3p expression was significantly lower in the combination treatment of EGCG and the miR-27a-3p inhibitor than in the individual inhibitor treatment in this study. The anticancer potency of the miR-27a-3p inhibitor was also revealed against MDA-MB-231 cells, supporting miRNA therapeutics against cancer. Furthermore, EGCG-modulated miR-27a-3p affected key Wnt/β-catenin pathway markers, causing signal suppression, including suppression of a key Wnt-targeted gene and the G1 phase regulator cyclin-D1, which also indicated its potential against breast cancer. Discussion These results signify the therapeutic potential of EGCG and its potential implementation through the miR-27a/Wnt/β-catenin pathway axis, resulting in reduced breast cancer proliferation, metastasis, and relapse.