Fig. 6. Effects of circATXN7 on immunotherapy efficacy.

A, B Tumor growth and survival curves of MC38K subcutaneous xenografts in WT (A) or circAtxn7^CKO (B) mice treated with anti-PD1 antibodies or IgG isotype control antibodies (n = 5 animals). C Schematic diagram showing circAtxn7 silencing in OT-I CD8⁺ T cells and ACT therapy against MC38K-OVA tumors. D 7.5 × 10⁵ OT-I cells transduced with GFP-tagged shcircAtxn7 were mixed with 7.5 × 10⁵ OT-I cells transduced with mCherry-tagged shVec, and co-injected intravenously into MC38K-OVA tumor-bearing mice, followed by flow cytometric analyses of the proportion of OT-I cells in total CD8⁺ cells at the indicated time points. E Quantification of OT-I cell number relative to total CD8⁺ cells (n = 3 samples). F–H 1.5 × 10⁶ OT-I cells with circAtxn7 silencing or shVec were transferred into MC38K-OVA tumor-bearing mice (n = 5 animals). At 20 days after transfer, MC38K-OVA tumors were subjected to analyses of CD8 IHC staining (F), tumor growth curves during the course (G), and weights (H). Scale bars, 50 μm. I Scheme of the preparation and adoptive transfer of tumor-reactive CD8⁺ T cells into autologous CRC PDXs. J Biodistribution of tumor-reactive CD8⁺ T cells 21 days after transfer. K Representative IHC staining for CD8 in harvested CRC PDX samples 21 days after transfer. Scare bars: 50 μm. L NF-κB activity in tumor-infiltrating CD8⁺ T cells purified from ACT-treated PDXs 21 days after transfer (n = 3 samples). M Growth curves of ACT-treated PDXs (n = 5 animals). N Weights of ACT-treated PDXs measured 21 days after transfer (n = 5 animals). Ut, cells without any treatment (G, H, and M, N). Statistical data presented in this figure show mean values ± SD (A, B, E, G, H, M, N). ***p ≤ 0.001, ****p ≤ 0.0001 and ns indicates p > 0.05, by two-tailed Student’s t-test (left panels of A, B, and E), one-way ANOVA (G, H, and M, N), or two-sided log-rank test (right panels of A, B). Source data and exact p values are provided as a Source Data file.