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However, cancer cells often evade these responses by overexpressing immune checkpoint regulators, such as PD-L1. Here, we identify the SNF2-family DNA translocase SMARCAL1 as a factor that favors tumor immune evasion by a dual mechanism involving both the suppression of innate immune signaling and the induction of PD-L1-mediated immune checkpoint responses. Mechanistically, SMARCAL1 relieves endogenous DNA damage and suppresses cGAS-STING-dependent signaling during cancer cell growth. Simultaneously, it cooperates with the AP-1 family member JUN to maintain chromatin accessibility at a transcriptional regulatory element in the PD-L1 gene, thereby promoting PD-L1 expression in cancer cells. SMARCAL1 loss hinders the ability of tumor cells to induce PD-L1 in response to genomic instability, enhances anti-tumor immune responses and sensitizes tumors to immune checkpoint blockade in a mouse melanoma model. Collectively, these studies uncover SMARCAL1 as a promising target for cancer immunotherapy. Overall design: Cleavage under targets and Release using nuclease (Cut-and-Run), for the chromatin profiling of SMARCAL1, JUN, H3K4me3 and H3K24me3 proteins in MDA-MB-436 cell lines treated as indicated."],"tag":["xref:PubMed:38301646"],"repository":["ENA"],"additional_accession":[]},"is_claimable":false,"name":"SMARCAL1 is a dual regulator of innate immune signaling and PD-L1 expression that promotes tumor immune evasion [CUT&RUN]","description":"SMARCAL1 is a dual regulator of innate immune signaling and PD-L1 expression that promotes tumor immune evasion [CUT&RUN]","dates":{"last_updated":"2025-09-24","first_public":"2024-01-26"},"accession":"PRJNA1028534","cross_references":{"GEO":["GSE245448"],"taxon":["9606"],"PubMed":["38301646"]}}