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Tractable In Vivo Reprogramming of Tumor Cells to Type 1 Conventional Dendritic Cell-like Cells
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Published on: August 1, 2025

The CARM1 epigenetic enzyme inhibits cross-presenting dendritic cell function in cancer immunity

Xixi Zhang1,2, Sherin Xirenayi3,4,5, Ye Zhao1

  • 1Department of Cancer Immunology and Virology, Dana-Farber Cancer Institute, Boston, MA, USA.

Science (New York, N.Y.)
|July 9, 2026
PubMed

Insights

Researchers identified the CARM1 enzyme as a key regulator of cancer immunity. Inhibiting CARM1 enhances the anti-tumor function of dendritic cells, offering a potential new cancer therapy target.

Area of Science:

  • Immunology
  • Epigenetics
  • Cancer Biology

Background:

  • The cancer-immunity cycle relies on type I conventional dendritic cells (cDC1s) for T cell-mediated immunity.
  • Current therapeutic strategies inadequately enhance intratumoral cDC1 function.
  • CARM1 (coactivator-associated arginine methyltransferase 1) is an epigenetic enzyme.

Purpose of the Study:

  • To investigate the role of CARM1 in regulating cDC1 function.
  • To explore CARM1 as a potential therapeutic target for enhancing anti-tumor immunity.

Main Methods:

  • Studied the effect of CARM1 inactivation on cDC1 antigen cross-presentation, activation, and tumor accumulation.
  • Utilized a CARM1 inhibitor in conjunction with a cancer neoantigen vaccine.
  • Analyzed chromatin accessibility changes at key regulatory sites (BATF3-Jun, RelA) following CARM1 inhibition.
  • Investigated the regulation of CARM1 expression by transforming growth factor-β.

Main Results:

  • CARM1 selectively inhibits cancer antigen presentation by cDC1s, but not cDC2s.
  • Carm1 gene inactivation enhanced cDC1 antigen cross-presentation, activation, and accumulation in tumors.
  • CARM1 inhibition boosted T cell priming mediated by cDC1s using a cancer neoantigen vaccine.
  • CARM1 inhibition increased chromatin accessibility at BATF3-Jun and RelA sites crucial for cDC1 function.
  • Transforming growth factor-β regulates Carm1 expression, suggesting CARM1 inactivation enhances function without disrupting homeostasis.

Conclusions:

  • CARM1 is a negative regulator of cDC1 anti-tumor function.
  • CARM1 inhibition represents a promising therapeutic strategy to enhance intratumoral cDC1 activity.
  • Targeting CARM1 could improve cancer immunotherapy outcomes in both mouse and human systems.

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