ICAM2 loss drives 5-fluorouracil resistance via TGF-β/Smad/SP1/PTN-dependent apoptosis evasion and macrophage remodeling in gastric cancer - PubMed
7 days ago
- #Chemoresistance
- #TGF-β Signaling
- #Gastric Cancer
- ICAM2 loss drives 5-fluorouracil resistance in gastric cancer via TGF-β/Smad/SP1/PTN-dependent apoptosis evasion and macrophage remodeling.
- Low ICAM2 expression correlates with poor NACT response, advanced tumor stage, worse differentiation, and reduced survival in AGC patients.
- Pre-NACT serum ICAM2 shows high predictive accuracy (AUC = 0.876) in distinguishing chemotherapy responders from non-responders.
- ICAM2 knockdown confers 5-FU resistance by inhibiting caspase-dependent apoptosis and promoting M2 macrophage polarization.
- Loss of ICAM2 activates TGF-β/Smad pathway, leading to SP1-mediated PTN upregulation, enhancing GC cell survival and M2 macrophage polarization.
- Targeted inhibition of TGF-β signaling reverses ICAM2-associated chemoresistance in cell culture and xenograft models.