ICAM2 loss drives 5-fluorouracil resistance via TGF-β/Smad/SP1/PTN-dependent apoptosis evasion and macrophage remodeling in gastric cancer

Figure 2 Intercellular adhesion molecule 2 knockdown enhances 5-fluorouracil resistance in gastric cancer cells by inhibiting caspase-dependent apoptosis. A: Half-maximal inhibitory concentration values for 5-fluorouracil (5-FU) in gastric cancer (GC) cells with intercellular adhesion molecule 2 (ICAM2) overexpression or knockdown; B: Colony formation assay in GC cells treated with varying 5-FU concentrations after ICAM2 overexpression or silencing; C: Growth curves of GC cells with ICAM2 overexpression or knockdown cultured with 5-FU; D: Flow cytometric analysis of apoptosis in 5-FU-treated GC cells with ICAM2 overexpression or knockdown; E: Western blotting analysis of apoptosis-related proteins in 5-FU-treated GC cells with ICAM2 overexpression or knockdown. ^aP < 0.05; ^bP < 0.01; ^cP < 0.001; ^dP < 0.0001. 5-FU: 5-fluorouracil; IC₅₀: Half-maximal inhibitory concentration; ICAM2: Intercellular adhesion molecule 2.