Interleukin-22 promotes cancer stemness and chemotherapy resistance in colorectal cancer via epidermal growth factor receptor/extracellular signal-regulated kinase pathway

Figure 4 Effect of extracellular signal-regulated kinase inhibition on interleukin-22-induced colorectal cancer cell proliferation and oxaliplatin chemoresistance. A: Cell proliferation was assessed using a cell counting kit-8 assay across different treatment groups. Osimertinib (Osi), extracellular signal-regulated kinase (EGFR) inhibitor Osi, 10 nM; B: Western blot analysis showing the levels of epidermal growth factor receptors (EGFR), p-EGFR, protein kinase B (AKT), p-AKT, extracellular signal-regulated kinase (ERK), and p-ERK across different treatment groups. Data are represented as mean ± SE (n = 3). Statistical analysis was performed using one-way analysis of variance followed by Tukey’s post hoc test. ^aP < 0.01 vs Control group; ^bP < 0.01 vs Oxaliplatin (L-OHP) group; ^cP < 0.01 vs Interleukin-22 + L-OHP group. L-OHP: Oxaliplatin; IL-22: Interleukin-22; EGFR: Epidermal growth factor receptors; AKT: Protein kinase B; ERK: Extracellular signal-regulated kinase.