Epigallocatechin-3-gallate (EGCG), a major catechin in green tea, has shown significant chemopreventive effects against various cancers. EGCG functions as a potent antioxidant, antiangiogenic, and antitumor agent, modulating tumor cell response to chemotherapy. It induces apoptosis, promotes cell cycle arrest, and suppresses oncogenic transcription factors and pluripotency factors. EGCG inhibits tumor incidence and multiplicity in multiple organs, including liver, stomach, skin, lung, mammary gland, and colon. It also reduces DNMTs, proteases, and DHFR activities, affecting transcription of tumor suppressor genes (TSGs) and protein synthesis. EGCG's safety, low cost, and bioavailability make it a promising candidate for cancer prevention. Mechanistically, EGCG modulates signal transduction pathways such as JAK/STAT, MAPK, PI3K/AKT, Wnt, and Notch, and inhibits telomerase activity. It also affects cellular signaling cascades, including NF-κB, AP-1, and MAP kinases, which are involved in cancer progression. EGCG inhibits NF-κB activation, reduces TNF-α expression, and modulates the expression of pro-apoptotic and anti-apoptotic proteins. It induces apoptosis in cancer cells by activating caspases and inhibiting Bcl-2 family proteins. EGCG also inhibits COX-2 expression, which is associated with inflammation and cancer progression. Additionally, EGCG modulates phase I and II enzymes, inhibiting procarcinogens and enhancing detoxification. It inhibits EGFR signaling, which is crucial for cancer cell proliferation and survival. EGCG's ability to inhibit multiple molecular targets suggests its potential as a chemopreventive agent in cancer therapy.Epigallocatechin-3-gallate (EGCG), a major catechin in green tea, has shown significant chemopreventive effects against various cancers. EGCG functions as a potent antioxidant, antiangiogenic, and antitumor agent, modulating tumor cell response to chemotherapy. It induces apoptosis, promotes cell cycle arrest, and suppresses oncogenic transcription factors and pluripotency factors. EGCG inhibits tumor incidence and multiplicity in multiple organs, including liver, stomach, skin, lung, mammary gland, and colon. It also reduces DNMTs, proteases, and DHFR activities, affecting transcription of tumor suppressor genes (TSGs) and protein synthesis. EGCG's safety, low cost, and bioavailability make it a promising candidate for cancer prevention. Mechanistically, EGCG modulates signal transduction pathways such as JAK/STAT, MAPK, PI3K/AKT, Wnt, and Notch, and inhibits telomerase activity. It also affects cellular signaling cascades, including NF-κB, AP-1, and MAP kinases, which are involved in cancer progression. EGCG inhibits NF-κB activation, reduces TNF-α expression, and modulates the expression of pro-apoptotic and anti-apoptotic proteins. It induces apoptosis in cancer cells by activating caspases and inhibiting Bcl-2 family proteins. EGCG also inhibits COX-2 expression, which is associated with inflammation and cancer progression. Additionally, EGCG modulates phase I and II enzymes, inhibiting procarcinogens and enhancing detoxification. It inhibits EGFR signaling, which is crucial for cancer cell proliferation and survival. EGCG's ability to inhibit multiple molecular targets suggests its potential as a chemopreventive agent in cancer therapy.