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
Raffel et al., 2013)
Importantly, these hormonal, metabolic, and epigenetic mechanisms do not function independently but operate in a highly interconnected manner to regulate luteal physiology
Griendling, K
In addition, there are several other stress kinases that were found to regulate NRF2 nuclear localization by phosphorylation, including the ER stress kinase PERK and the energy sensor AMPK [13, 14]
doi: 10.1016/j.foodres.2023.112582 4 CharnchaiP.JantamaS