Information from the 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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Related topics: Immune cells in cancer · Histone Deacetylase Inhibitors Research · Chemokine receptors and signaling
Thai researcher and institutional participation
Wenqian Zhang · Ministry of Education
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