Loss of ARID1A leads to a cold tumor phenotype via suppression of IFNγ signaling.

ABSTRACT: The collapse of inflammatory signaling that recruits cytotoxic immune cells to the tumor microenvironment contributes to the immunologically cold tumor phenotype in neuroblastoma (NB) and is a barrier to NB immunotherapy. Multiple studies have reported that MYCN amplification, a trait of high-risk NB, correlates with a loss of inflammatory signaling; but MYCN also correlates with 1p36 deletions in NB where the SWI/SNF chromatin remodeling complex subunit ARID1A (1p36.11) is located. ARID1A is known to support inflammatory signaling in adult cancers but its role in NB inflammatory signaling is unexplored. We find MYCN overexpression causes a stronger inflammatory response to interferon-gamma (IFNγ). ARID1A knockdown causes a weaker inflammatory response and reduces IFNγ induced gene signatu

SUBMITTER: Watson PM 

PROVIDER: S-EPMC11906763 | biostudies-literature | 2025 Mar

REPOSITORIES: biostudies-literature