目的：肿瘤坏死因子受体II（TNFR2）广泛表达于包括结肠癌、非何杰金淋巴瘤、骨髓瘤、肾癌和卵巢癌在内的多种肿瘤细胞中，其确切作用有待完全理解。本研究旨在研究TNFR2遗传敲除对小鼠MC38和CT26结肠癌细胞在体内外生长的影响。方法：利用CRISPR/Cas9技术敲除小鼠MC38和CT26结肠癌细胞上的TNFR2。研究野生型（W.T.）和TNFR2缺乏型MC38和CT26细胞的体外生长和集落形成以及可能的机制。还检查了W.T.和TNFR2缺陷的MC38和CT26肿瘤在小鼠体内的生长和肿瘤内CD8 CTL的数量。结果：TNFR2缺陷削弱了癌细胞的体外增殖和集落形成，这与蛋白激酶B（AKT）磷酸化的抑制和自噬诱导的细胞死亡增加有关。此外，TNFR2的缺失也显著削弱了同种C57BL/6小鼠或BALB/c小鼠中MC38或CT26的体内生长，并伴随着循环中可溶性TNFR2水平的下降和肿瘤浸润IFNγ+ CD8细胞数量的增加。结论：TNFR2在小鼠结肠癌的生长中起着作用。我们的研究为支持开发TNFR2对抗剂用于癌症治疗提供了进一步的实验证据。©作者。

Objective: Tumor necrosis factor (TNF) receptor type II (TNFR2) is expressed by a wide spectrum of tumor cells including colon cancer, non-Hodgkin lymphoma, myeloma, renal carcinoma and ovarian cancer, and its exact role remains to be fully understood. In this study, we examined the effect of genetic ablation of TNFR2 on in vitro and in vivo growth of mouse MC38 and CT26 colon cancer cells. Methods: CRISPR/Cas9 technology was used to knockout TNFR2 on mouse MC38 and CT26 colon cancer cells. In vitro growth and colony formation of wild-type (W.T.) and TNFR2 deficiency of MC38 and CT26 cells, as well as the potential mechanism, was studied. The growth of W.T. and TNFR2 deficient MC38 and CT26 tumors in mice and intratumoral CD8 CTLs were also examined. Results: TNFR2 deficiency impaired in vitro proliferation and colony formation of cancer cells. This was associated with the inhibition of protein kinase B (AKT) phosphorylation and enhanced autophagy-induced cell death. Moreover, deficiency of TNFR2 also markedly impaired in vivo growth of MC38 or CT26 in the syngeneic C57BL/6 mice or BALB/c mice, respectively, accompanied by the decrease in soluble TNFR2 levels in the circulation and the increase in the number of tumor-infiltrating IFNγ+ CD8 cells. Conclusion: TNFR2 plays a role in the growth of mouse colon cancers. Our study provides further experimental evidence to support the development of TNFR2 antagonistic agents in the treatment of cancer.© The author(s).