Fig. 2

TNFAIP2 protects HNSCC cells from cisplatin-induced apoptosis by inhibiting ROS/JNK signaling. (a-b) Flow cytometry analyses of ROS in TNFAIP2-overexpressing FADU (a) and CAL33 cells (b). (c) Analyses of GSH/GSSG and SOD in TNFAIP2-overexpressing HNSCC cell lines. (d-e) Cisplatin IC50 evaluations in TNFAIP2-knockdown FADU (d) and CAL33 (e) cells with or without NAC (4 mmol/L, 2 h). (f-g) Flow cytometry analyses of cisplatin-induced apoptosis in TNFAIP2-knockdown FADU (f) and CAL33 (g) cells with or without NAC (4 mmol/L, 2 h). (h) Schematic diagram of ROS/JNK signaling in cisplatin-induced apoptosis. (i-j) Cisplatin IC50 evaluations in TNFAIP2-knockdown FADU (i) and CAL33 (j) cells with or without the JNK pathway inhibitor SP600125 (20 µmol/L, 2 h). (k) Western blot analysis of the molecular markers for JNK and apoptosis signaling induced by cisplatin in vector- or TNFAIP2-overexpressing HNSCC cell lines. (l) Western blot analysis of the molecular markers for JNK and apoptosis signaling induced by cisplatin in control or TNFAIP2 knockdown HNSCC cell lines with or without NAC (4 mmol/L, 2 h). Data are presented as the mean ± SEM. n.s., not significant; ** P < 0.01; *** P < 0.001. NAC, N-acetylcysteine