{"database":"iProX","file_versions":[],"scores":null,"additional":{"omics_type":["Proteomics"],"submitter":["Zhidong Gao"],"species":["Mus Musculus"],"full_dataset_link":["http://www.iprox.org/page/project.html?id=IPX0016693000"],"submitter_email":["gaozhidong@pkuph.edu.cn"],"submitter_affiliation":["Peking University People’s Hospital"],"sample_protocol":[""],"repository":["iProX"],"data_protocol":[""],"pubmed_abstract":["Microsatellite-stable/proficient mismatch repair (MSS/pMMR) colorectal cancer (CRC) is characterized by a cold tumor microenvironment, with limited CD8⁺ T cell infiltration and poor responsiveness to immune checkpoint inhibitors (ICIs). Here, using an in vivo CRISPR/Cas9 screen in a CMT93 cell-derived murine tumor model, we identify Arid3b as a key negative regulator of CD8⁺ T cell infiltration and antitumor activity. Genetic ablation of Arid3b in CD8⁺ T cells significantly enhances their intratumoral accumulation and promotes robust tumor control. Mechanistically, Arid3b deficiency upregulates Runx3, driving a tissue-resident memory-like phenotype and effector function. Notably, the benefits conferred by Arid3b deficiency are abrogated upon Runx3 deletion, indicating a RUNX3-dependent mechanism. Together, targeting ARID3B could offer a promising strategy to reshape the tumor microenvironment and sensitize MSS CRC to immunotherapy."],"pubmed_title":["Arid3b suppresses CD8 + T cell infiltration and function in microsatellite-stable colorectal cancer via Runx3."],"pubmed_authors":["Wang Shuo S, Hou Sen S, Luo Ce C, Zhang Haorui H, Jin Yiteng Y, Zhang Rui R, Zhao Yanping Y, Xiong Xiaoyu X, Guo Rui R, Wang Chao C, Bao Yudi Y, Wen Liang L, Pan Deng D, Ye Yingjiang Y, Zeng Zexian Z, Gao Zhidong Z"],"additional_accession":[]},"is_claimable":false,"name":"Arid3b suppresses CD8+ T cell infiltration and function in Microsatellite-stable colorectal cancer via Runx3","description":"Microsatellite stable/proficient mismatch repair (MSS/pMMR) colorectal cancer (CRC) is characterized by a cold tumor microenvironment, marked by sparse CD8⁺ T cell infiltration and resistance to immune checkpoint inhibitors (ICIs). To uncover regulators that limit CD8⁺ T cell infiltration in MSS CRC, we conducted an in vivo CRISPR/Cas9 screen targeting genes in CD8⁺ T cells using a CMT93 cell-derived tumor model. This screen identified Arid3b as a key negative regulator of CD8⁺ T cell tumor infiltration and antitumor activity. Genetic ablation of Arid3b in CD8⁺ T cells significantly enhanced their intratumoral accumulation and mediated robust tumor control. Mechanistically, Arid3b deficiency upregulated Runx3, promoting a tissue-resident memory phenotype and effector function. Notably, the benefits conferred by Arid3b knockout were abrogated by Runx3 deletion, indicating a Runx3-dependent mechanism. In summary, targeting ARID3B could offer a promising strategy to reshape the tumor microenvironment and sensitize MSS CRC to immunotherapy.","dates":{"publication":"Thu Apr 16 00:00:00 GMT+01:00 2026"},"accession":"PXD077233","cross_references":{"TAXONOMY":["10090"],"pubmed":["42140952"]}}