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KRAS-IRF2 Axis Drives Immune Suppression and Immune Therapy Resistance in Colorectal Cancer
Abstract
The biological functions and mechanisms of oncogenic KRASG12D(KRAS) in resistance to immune check-point blockade (ICB) therapy are not fully understood. We demonstrate that KRAS* represses the expressionof interferon regulatory factor 2 (IRF2), which in turn directly represses CXCL3 expression. KRAS*-mediatedrepression of IRF2 results in high expression of CXCL3, which binds to CXCR2 on myeloid-derived suppres-sor cells and promotes their migration to the tumor microenvironment. Anti-PD-1 resistance of KRAS-ex-pressing tumors can be overcome by enforced IRF2 expression or by inhibition of CXCR2. Colorectal cancer(CRC) showing higher IRF2 expression exhibited increased responsiveness to anti-PD-1 therapy. The KRAS-IRF2-CXCL3-CXCR2 axis provides a framework for patient selection and combination therapies to enhancethe effectiveness of ICB therapy in CRC
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