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This resistance is generally attributed to the limited antigen presentation of heterogeneous cells within tumors. Here, we aimed to isolate and characterize these diverse subgroups of tumor post\u2010RT to understand the molecular mechanisms of their resistance to ICB.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">Single\u2010cell RNA\u2010sequencing (scRNA\u2010seq) was used to profile senescent cancer cell clusters induced by RT in LNCaP cells. The expression and phosphorylation levels of ataxia telangiectasia and Rad3\u2010related protein (ATR) were assessed by immunohistochemistry in clinical samples from patients with or without RT. Co\u2010immunoprecipitation, mutagenesis, and Western blotting were used to measure the interactions between proteins. Xenograft experiments were performed to assess the tumor immune response in the mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">We identified a subset of PCa cells that exhibited resistance to RT, characterized by a reduced antigen presentation capability, which enhanced their ability to evade immune detection and resist cytotoxic T\u2010lymphocyte\u2010associated protein 4 (CTLA\u20104) blockade. scRNA\u2010seq revealed that the senescent state was a transient phase of PCa cells post\u2010RT, particularly in CTLA\u20104 blockade treatment\u2010resistant cells. This state was marked by increased cytosolic ATR level. Cytosolic ATR phosphorylated CD86 in its cytosolic domain and enhanced the interaction between CD86 and its E3 ligase MARCH1 through electrostatic attraction. Depletion or inhibition of Atr increased the sensitivity to immune attack and improved responses to anti\u2010Ctla\u20104 antibody treatment in a mouse model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Our findings indicate that the activation of cytosolic ATR, which is associated with cellular senescence, impedes the effectiveness of combined RT and ICB treatments. This discovery may provide valuable insights for improving the efficacy of combined RT and ICB therapies in PCa.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/cac2.12636","type":"journal-article","created":{"date-parts":[[2024,12,19]],"date-time":"2024-12-19T06:13:13Z","timestamp":1734588793000},"page":"218-244","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Radiotherapy\u2010resistant prostate cancer cells escape immune checkpoint blockade through the senescence\u2010related ataxia telangiectasia and Rad3\u2010related protein"],"prefix":"10.34133","volume":"45","author":[{"given":"Chenyi","family":"Shao","sequence":"first","affiliation":[{"name":"Chinese Academy of Medical Sciences and Peking Union Medical College","place":["Tianjin, P. R. 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