ArticleCell death & disease2026
CXCR2 blockade potentiates HDAC3 deletion mediated antitumor immunity in colorectal cancer.
Article in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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10 authors.
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Abstract
HDAC3 is highly expressed in colorectal cancer (CRC) and associated with poor prognosis. This study reveals that HDAC3 deletion dually regulates chemokine expression through epigenetic mechanisms, promoting CD8⁺ T cell infiltration (via CXCL10) on one hand, while enhancing the recruitment of myeloid-derived suppressor cells (MDSCs) (via CXCL1/2/3/5) on the other. The latter, mediated through CXCR2 signaling, counteracts the intrinsic anti-tumor effect of HDAC3 deletion. We further demonstrate that combining a CXCR2 inhibitor effectively blocks MDSC infiltration and significantly enhances the immunotherapeutic efficacy mediated by HDAC3 deletion. This study systematically elucidates the "double-edged sword" role of HDAC3 in the CRC immune microenvironment and provides a theoretical and experimental basis for an HDAC3/CXCR2 dual-targeting therapeutic strategy.
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