Extended Data Fig. 3: (related to Fig. 1). Targeting PTPN2 in VDAC2-deficient tumour cells enhanced anti-tumour immunity.
From: VDAC2 loss elicits tumour destruction and inflammation for cancer therapy
a, Control, VDAC2-deficient or PTPN2-deficient B16-OVA tumour cell viability after co-culture with OT-I cells at indicated E:T ratios for 36 h (n = 3 per group). b, Real-time survival analysis of indicated B16-OVA tumour cells after treatment with 1 ng ml–1 (left) or 10 ng ml–1 (right) of IFNγ (n = 5 for sgNTC in 1 ng ml–1 treatment group; n = 6 for other groups for both panels). c, C57BL6 mice were inoculated with indicated B16-OVA tumour cells, followed by treatment of tumour-bearing mice with isotype control (left panels) or anti-PD-L1 antibody (right panels) at days 7, 10, and 13 after tumour inoculation (n = 7 for isotype-treated groups; n = 8 for anti-PD-L1-treated groups). Tumour growth (first and third panels) and mouse survival (second and fourth panels) were monitored. d, Immunoblot analysis of VDAC2 and PTPN2 expression in control, VDAC2-deficient, PTPN2-deficient or VDAC2 and PTPN2 co-deficient B16-OVA tumour cells. e, Real-time survival analysis of indicated B16-OVA tumour cells after treatment with 1 ng ml–1 of IFNγ (n = 2 per group). f, C57BL/6 mice were inoculated with indicated B16-OVA tumour cells (n = 8 for sgNTC + sgNTC; 9 for all other groups). Tumour growth (left) and mouse survival (right) were monitored. Data are representative of three (a), two (b, e, f) or one (c, d) independent experiments and are mean ± s.e.m. One-way ANOVA (a). Two-way ANOVA (b; tumour size of c, f). Mantel−Cox test (survival of c, f).
