<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Huang Q</submitter><funding>National Key R&amp;amp;D Program of China</funding><funding>National Natural Science Founding of China grants</funding><funding>Shanghai Frontiers Science Center of Cellular Homeostasis and Human Diseases, the Innovation Program of Shanghai Municipal Education Commission</funding><funding>Shanghai Municipal Commission of Health and Family Planning</funding><funding>Innovative research team of high-level local universities in Shanghai</funding><pagination>e178079</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11601948</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>134(23)</volume><pubmed_abstract>Ku70, a DNA repair protein, binds to the damaged DNA ends and orchestrates the recruitment of other proteins to facilitate repair of DNA double-strand breaks. Besides its essential role in DNA repair, several studies have highlighted nonclassical functions of Ku70 in cellular processes. However, its function in immune homeostasis and antitumor immunity remains unknown. Here, we discovered a marked association between elevated Ku70 expression and unfavorable prognosis in lung adenocarcinoma, focusing specifically on increased Ku70 levels in tumor-infiltrated Tregs. Using a lung-colonizing tumor model in mice with Treg-specific Ku70 deficiency, we demonstrated that deletion of Ku70 in Tregs led to a stronger antitumor response and slower tumor growth due to impaired immune-suppressive capaci</pubmed_abstract><journal>The Journal of clinical investigation</journal><pubmed_title>Nonclassical action of Ku70 promotes Treg-suppressive function through a FOXP3-dependent mechanism in lung adenocarcinoma.</pubmed_title><pmcid>PMC11601948</pmcid><funding_grant_id>82241222</funding_grant_id><funding_grant_id>82271829</funding_grant_id><funding_grant_id>2023ZD0501605</funding_grant_id><funding_grant_id>202040117</funding_grant_id><funding_grant_id>SHSMU-ZDCX20210601</funding_grant_id><funding_grant_id>21140902900</funding_grant_id><funding_grant_id>32130041</funding_grant_id><funding_grant_id>2023ZD0507404</funding_grant_id><funding_grant_id>31961133011</funding_grant_id><funding_grant_id>2019YFA09006102</funding_grant_id><pubmed_authors>Zhou Q</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Li D</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Du Y</pubmed_authors><pubmed_authors>Huang Q</pubmed_authors><pubmed_authors>Ye Y</pubmed_authors><pubmed_authors>Dai X</pubmed_authors><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Zhang W</pubmed_authors><pubmed_authors>Chen Z</pubmed_authors><pubmed_authors>Song S</pubmed_authors><pubmed_authors>Li B</pubmed_authors><pubmed_authors>Tian N</pubmed_authors><pubmed_authors>Cheng H</pubmed_authors><pubmed_authors>Dai SM</pubmed_authors><pubmed_authors>Liang R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Nonclassical action of Ku70 promotes Treg-suppressive function through a FOXP3-dependent mechanism in lung adenocarcinoma.</name><description>Ku70, a DNA repair protein, binds to the damaged DNA ends and orchestrates the recruitment of other proteins to facilitate repair of DNA double-strand breaks. Besides its essential role in DNA repair, several studies have highlighted nonclassical functions of Ku70 in cellular processes. However, its function in immune homeostasis and antitumor immunity remains unknown. Here, we discovered a marked association between elevated Ku70 expression and unfavorable prognosis in lung adenocarcinoma, focusing specifically on increased Ku70 levels in tumor-infiltrated Tregs. Using a lung-colonizing tumor model in mice with Treg-specific Ku70 deficiency, we demonstrated that deletion of Ku70 in Tregs led to a stronger antitumor response and slower tumor growth due to impaired immune-suppressive capaci</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Oct</publication><modification>2026-06-02T23:10:25.825Z</modification><creation>2025-04-06T01:57:19.25Z</creation></dates><accession>S-EPMC11601948</accession><cross_references><pubmed>39446493</pubmed><doi>10.1172/JCI178079</doi></cross_references></HashMap>