Fig. 7.

TNFAIP8 regulates NSCLC proliferation and chemoresistance in vivo. Mice were treated with cisplatin (3.0 mg/kg body weight; i.p., three times per week) or with 0.1 ml of PBS (pH 7.4; i.p., three times per week). a Representative features of tumours at 28 days after inoculation using A549/Ctrl or A549/TNFAIP8-sh2 cells treated with PBS or cisplatin. b Tumours growth in the mice injected with A549/Ctrl or A549/TNFAIP8-sh2 cells treated with PBS or cisplatin. Inoculations were performed in 10 mice. c Tumour volumes at day 28 after the inoculation. Left (black column), average tumour volumes at day 28 after inoculation with A549/Ctrl or A549/TNFAIP8-sh2 cells in mice treated with PBS; right (white column), average tumour volumes at day 28 after inoculation of A549/Ctrl or A549/TNFAIP8-sh2 cells in mice treated with cisplatin. d qRT-PCR and Western blot analysis of the relative p53 expression in tumours originating from A549/Ctrl or A549/TNFAIP8-sh2 cells treated with PBS or cisplatin. Data are presented as the mean ± SEM (n = 3). e Proposed model for TNFAIP8-induced proliferation and cisplatin resistance in NSCLC. TNFAIP8-mediated p53 suppression activates the expression of cyclin D1 and RAD51, thus promoting cell cycle progression and DNA repair. These actions lead to NSCLC cell proliferation and cisplatin resistance