Epigallocatechin gallate (EGCG), a polyphenolic compound found in green tea, has shown significant potential as an anticancer agent by targeting various cancer hallmarks. This review summarizes the mechanisms by which EGCG exerts its anticancer effects, including its ability to inhibit cell proliferation, induce apoptosis, suppress angiogenesis, and prevent metastasis. EGCG targets key cancer hallmarks such as sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, replicative immortality, induction of angiogenesis, activation of invasion and metastasis, reprogramming of energy metabolism, and evasion of immune destruction. EGCG achieves these effects through multiple pathways, including the modulation of signaling molecules like ERK, PI3K-Akt, and NF-κB, as well as the inhibition of telomerase activity and the induction of apoptosis via both caspase-dependent and caspase-independent mechanisms. Additionally, EGCG has been shown to inhibit tumor-associated immune evasion by modulating immune checkpoints such as PD-1 and PD-L1. Despite its promising therapeutic potential, EGCG faces challenges related to its low bioavailability, which is influenced by factors such as intestinal metabolism and poor absorption. Strategies to enhance EGCG bioavailability, including the use of nano-delivery systems and co-administration with other compounds like curcumin and piperine, are being explored. While EGCG shows promise as a natural therapeutic agent, further research is needed to fully understand its mechanisms and to develop effective clinical applications.Epigallocatechin gallate (EGCG), a polyphenolic compound found in green tea, has shown significant potential as an anticancer agent by targeting various cancer hallmarks. This review summarizes the mechanisms by which EGCG exerts its anticancer effects, including its ability to inhibit cell proliferation, induce apoptosis, suppress angiogenesis, and prevent metastasis. EGCG targets key cancer hallmarks such as sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, replicative immortality, induction of angiogenesis, activation of invasion and metastasis, reprogramming of energy metabolism, and evasion of immune destruction. EGCG achieves these effects through multiple pathways, including the modulation of signaling molecules like ERK, PI3K-Akt, and NF-κB, as well as the inhibition of telomerase activity and the induction of apoptosis via both caspase-dependent and caspase-independent mechanisms. Additionally, EGCG has been shown to inhibit tumor-associated immune evasion by modulating immune checkpoints such as PD-1 and PD-L1. Despite its promising therapeutic potential, EGCG faces challenges related to its low bioavailability, which is influenced by factors such as intestinal metabolism and poor absorption. Strategies to enhance EGCG bioavailability, including the use of nano-delivery systems and co-administration with other compounds like curcumin and piperine, are being explored. While EGCG shows promise as a natural therapeutic agent, further research is needed to fully understand its mechanisms and to develop effective clinical applications.