Fig. 5: The function of EPHA5 in pro-proliferation and anti-apoptosis at least partly depend on the STAT3 signaling pathway in vivo and in vitro.

A Western blot analysis of p-STAT3, STAT3, PCNA, Caspase-3, Cleaved-caspase-3, β-actin in FTC-133 and FTC-238 cells. **p < 0.01, ^##p < 0.01, n = 3. B Colony formation assay of FTC-133 and FTC-238 cells. **p < 0.01, ^##p < 0.01, n = 6. C Representative TUNEL staining of FTC cells; the nuclei were stained with DAPI. Scale bar = 200 μm. TUNEL scores. The relative number of apoptotic cells is represented as TUNEL-positive cells/DAPI. *p < 0.05, ^##p < 0.01, n = 6. D Western blot analysis of STAT3, cleaved-caspase-3, and β-actin in FTC-133 and FTC-238 cells. **p < 0.01, n = 3. E Colony formation assay of FTC-133 and FTC-238 cells transfected with si-NC or si-EPHA5 or si-EPHA5 + si-STAT3 respectively. **p < 0.01, n = 3. F Representative FITC and PI staining of FTC cells. Scale bar, 200 μm. The relative number of apoptotic cells is represented as FITC-positive cells ratio. *p < 0.05, n = 3. G Images of the xenograft tumors formed in nude mice subcutaneously injected with FTC-238 cells with EPHA5 knockdown or overexpression treated with SH-4-54. H, I Tumor weight was measured after the tumors were removed. Tumor growth curves were measured after injection of FTC238 cells with EPHA5 knockdown or EPHA5 overexpression treated with SH-4-54. *p < 0.05, ^##p < 0.01, n = 5.