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Additionally, ESC suppresses epithelial-mesenchymal transition (EMT) by decreasing mesenchymal markers (Vimentin, N-cadherin) and increasing epithelial marker (E-cadherin).(Bottom left)In endometrial cancer (EC), ESC directly binds to heterogeneous nuclear ribonucleoprotein A1 (hnRNPA1), blocking nuclear export of anti-apoptotic mRNAs (BCLXL, XIAP), which remain trapped in the nucleus, thereby preventing their translation and inducing apoptosis.(Bottom right)In breast cancer, ESC delivered via chitosan nanoparticles reduces pro-tumorigenic factors (VEGF, NF-B, Cyclin D1) while enhancing antioxidant defenses (SOD, CAT, GPx), leading to tumor growth inhibition.(Bottom panel)Common anticancer mechanisms shared across cancer types include ROS-mediated mitochondrial apoptosis, NF-B suppression, PI3K/Akt pathway inhibition, cell cycle arrest at G1/S checkpoint, and p53 activation

Accumulation of free ADP-ribose from mitochondria mediates oxidative stress-induced gating of TRPM2 cation channels

85 263272 (Academic Press, 2019)

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