| Literature DB >> 31239318 |
Lulu Shao1,2, Weizhou Hou1, Nicole E Scharping3,4, Frank P Vendetti5, Rashmi Srivastava1,2, Chandra Nath Roy1,2, Ashley V Menk3,4, Yiyang Wang3,4, Joe-Marc Chauvin4, Pooja Karukonda5, Stephen H Thorne1, Veit Hornung6, Hassane M Zarour4, Christopher J Bakkenist5, Greg M Delgoffe3,4, Saumendra N Sarkar7,2,4.
Abstract
Multiple studies have associated the transcription factor IRF1 with tumor-suppressive activities. Here, we report an opposite tumor cell-intrinsic function of IRF1 in promoting tumor growth. IRF1-deficient tumor cells showed reduced tumor growth in MC38 and CT26 colon carcinoma and B16 melanoma mouse models. This reduction in tumor growth was dependent on host CD8+ T cells. Detailed profiling of tumor-infiltrating leukocytes did not show changes in the various T-cell and myeloid cell populations. However, CD8+ T cells that had infiltrated IRF1-deficieint tumors in vivo exhibited enhanced cytotoxicity. IRF1-deficient tumor cells lost the ability to upregulate PD-L1 expression in vitro and in vivo and were more susceptible to T-cell-mediated killing. Induced expression of PD-L1 in IRF1-deficient tumor cells restored tumor growth. These results indicate differential activity of IRF1 in tumor escape. ©2019 American Association for Cancer Research.Entities:
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Year: 2019 PMID： 31239318 PMCID： PMC6677597 DOI： 10.1158/2326-6066.CIR-18-0711
Source DB: PubMed Journal: Cancer Immunol Res ISSN： 2326-6066 Impact factor: 12.020