{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T08:31:43Z","timestamp":1782981103416,"version":"3.54.5"},"reference-count":53,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T00:00:00Z","timestamp":1781136000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Oncol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>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\/\u03b2-catenin pathway markers were examined to further establish the therapeutic route of EGCG via the miR-27a\/Wnt\/\u03b2-catenin pathway axis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Result<\/jats:title>\n                    <jats:p>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\/\u03b2-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.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>These results signify the therapeutic potential of EGCG and its potential implementation through the miR-27a\/Wnt\/\u03b2-catenin pathway axis, resulting in reduced breast cancer proliferation, metastasis, and relapse.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fonc.2026.1835026","type":"journal-article","created":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T05:49:06Z","timestamp":1781156946000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["Epigallocatechin-3-gallate suppressed 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