Fig. 4: USP29 promotes chemoresistance in gastric cancer by enhancing FSP1 mediated ferroptosis inhibition.

a Immunoblots of FSP1 and USP29 in AGS-R cells stably expressing control or two independent USP29 sgRNAs. b Percentage of C11-BODIPY-positive cells in cells from (a) with/without 24-h cisplatin (2 μM) treatment. c Survival fraction of cells from (a) exposed to cisplatin at the indicated dose for 2 weeks. d Immunoblots of FSP1 and USP29 in AGS-R cells stably expressing control or USP29 sgRNA transfected with USP29 WT or CI vectors. e Percentage of C11-BODIPY-positive cells in cells from (d) with/without 24-h cisplatin (2 μM) treatment. f Survival fraction of cells from (d) exposed to cisplatin at the indicated dose for 2 weeks. g Immunoblots of FSP1 and USP29 in AGS-R cells stably expressing the indicated vectors. h Percentage of C11-BODIPY-positive cells in cells from (g) with/without 24-h cisplatin (2 μM) treatment. i Survival fraction of cells from (g) exposed to cisplatin at the indicated dose for 2 weeks. j Survival fraction of control or USP29-knockout AGS-R cells exposed to cisplatin at the indicated dose combining with/without the indicated reagents for 2 weeks. k Growth curves of the AGS-R xenograft tumor models with the indicated treatment. l Quantification of the weight of the tumors in different groups of the xenograft tumor models. Experiment was repeated 3 times, and representative blots are presented in (a, d, g). Data shown represent mean ± SD from three independent experiments in (b, c, e, f, h–j), or from one representative experiment of 5 mice per group in (k, l). P values are determined by 1-way ANOVA in (b, e, h, l), or 2-way ANOVA in (c, f, i–k). The survival fraction was calculated as the ratio of colony-forming cells with the indicated treatment to those in the untreated control group. NS, not significant. Source data are provided as Source Data file.