Introduction

Green tea catechins, particularly epigallocatechin‐3‐gallate (EGCG), have drawn significant scientific attention due to their promising anticancer properties. Multiple peer‐reviewed studies (from 2015 to 2025) detail how catechins interfere with various cancer pathways—from inducing apoptosis and inhibiting angiogenesis to regulating the cell cycle and modulating metabolic and epigenetic processes.

Molecular Pathways Targeted by Catechins

Multiple studies using in vitro and in vivo models have identified several key molecular pathways that catechins, and especially EGCG, target within cancer cells. The evidence consistently demonstrates that catechins interfere with free radical levels, cell survival signals, and proliferation. Major mechanisms include:

• Apoptosis Induction:
  Catechins regulate apoptotic pathways—by triggering PARP cleavage, caspase activation, and modulating the Bax/Bcl-2 ratio—as seen in studies on HepG2 and nasopharyngeal carcinoma (NPC) cells (ScienceDirect1; Frontiers2).

• Angiogenesis Inhibition:
  EGCG suppresses angiogenesis primarily through inhibition of vascular endothelial growth factor (VEGF) and its receptor (VEGFR2). This effect reduces blood supply to tumors and hampers metastatic potential (PubMed3; PMC4).

• Cell Cycle Regulation:
  By modulating cyclins and cyclin‐dependent kinases (CDKs), EGCG induces cell cycle arrest at critical checkpoints (G1/S or G2/M phases), thereby halting uncontrolled cell proliferation (Frontiers2).

• Metabolic and De Novo Lipogenesis Pathway Inhibition:
  In HepG2 cells, EGCG has been reported to inhibit de novo lipogenesis by downregulating enzymes such as fatty acid synthase (FASN) and ATP-citrate lyase (ACLY), leading to energy metabolism disruption and cell death (BMC Cancer5).

• Epigenetic Modulation:
  Catechins can alter epigenetic markers by inhibiting DNA methyltransferases (DNMT) and histone deacetylases (HDAC), reactivating tumor suppressor genes and enhancing cancer cell susceptibility to apoptosis (PMC6).

• Reactive Oxygen Species (ROS) Balance:
  EGCG exhibits dual antioxidant and pro-oxidant effects. By modulating ROS levels, it can tip the balance toward cell death in tumor cells while protecting normal cells (MDPI7).

Comparative Efficacy: EGCG Versus Other Catechins

EGCG is consistently recognized as the most effective catechin in anticancer studies. Key factors include:

• Structural Advantages:
  With eight hydroxyl groups, EGCG demonstrates superior target binding compared to other catechins such as epicatechin and epicatechin gallate (PMC8).

• Enhanced Potency:
  Experimental data indicate that EGCG has a significantly lower IC50 than other catechins (e.g., 0.5 mM versus 3.0 mM in HepG2 cells) and is more potent in ROS generation and apoptosis induction (BMC Cancer5; MDPI7).

• Broader Molecular Targeting:
  While all catechins inhibit tumor progression, EGCG uniquely affects a broader spectrum of molecular pathways such as SIRT1 downregulation to activate the p53 pathway, contributing to apoptosis in NPC cells (Frontiers2).

The Takeaway

• EGCG, a green tea catechin, exhibits anticancer effects by inducing apoptosis (via PARP cleavage, caspase activation, and altering the Bax/Bcl-2 ratio), inhibiting angiogenesis (through suppression of VEGF and VEGFR2), regulating the cell cycle, and modulating metabolic and epigenetic processes.
• Comparative studies show that EGCG is more potent than other catechins, having a lower IC50 (e.g., 0.5 mM vs 3.0 mM in HepG2 cells) and targeting a broader range of molecular pathways including SIRT1 downregulation to activate the p53 pathway.