{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zang Y"],"funding":["Tippins Foundation","NIDDK NIH HHS","UPMC Hillman Cancer Center Animal Facility and the Tissue and Research Pathology Services","NCI NIH HHS","Mellam Family Foundation","NIGMS NIH HHS"],"pagination":["198-207"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5761340"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["415"],"pubmed_abstract":["ELL2 is an androgen-responsive gene that is expressed by prostate epithelial cells and is frequently down-regulated in prostate cancer. Deletion of Ell2 in the murine prostate induced murine prostatic intraepithelial neoplasia and ELL2 knockdown enhanced proliferation and migration in C4-2 prostate cancer cells. Here, knockdown of ELL2 sensitized prostate cancer cells to DNA damage and overexpression of ELL2 protected prostate cancer cells from DNA damage. Knockdown of ELL2 impaired non-homologous end joining repair but not homologous recombination repair. Transfected ELL2 co-immunoprecipitated with both Ku70 and Ku80 proteins. ELL2 could bind to and co-accumulate with Ku70/Ku80 proteins at sites of DNA damage. Knockdown of ELL2 dramatically inhibited Ku70 and Ku80 recruitment and retentio"],"journal":["Cancer letters"],"pubmed_title":["ELL2 regulates DNA non-homologous end joining (NHEJ) repair in prostate cancer cells."],"pmcid":["PMC5761340"],"funding_grant_id":["R01 GM118833","P30 CA047904","1R50CA211242","P50 CA180995","P30CA047904","9R01CA186780","T32 DK007774","1P50CA180995","R50 CA211242","R01 CA186780"],"pubmed_authors":["Xue B","Nelson JB","Zang Y","Zhou Y","Yang D","Ai J","Shan Y","Qiu X","Pascal LE","Wang S","Lan L","Wang Z","Wei L","Zhong M"],"additional_accession":[]},"is_claimable":false,"name":"ELL2 regulates DNA non-homologous end joining (NHEJ) repair in prostate cancer cells.","description":"ELL2 is an androgen-responsive gene that is expressed by prostate epithelial cells and is frequently down-regulated in prostate cancer. Deletion of Ell2 in the murine prostate induced murine prostatic intraepithelial neoplasia and ELL2 knockdown enhanced proliferation and migration in C4-2 prostate cancer cells. Here, knockdown of ELL2 sensitized prostate cancer cells to DNA damage and overexpression of ELL2 protected prostate cancer cells from DNA damage. Knockdown of ELL2 impaired non-homologous end joining repair but not homologous recombination repair. Transfected ELL2 co-immunoprecipitated with both Ku70 and Ku80 proteins. ELL2 could bind to and co-accumulate with Ku70/Ku80 proteins at sites of DNA damage. Knockdown of ELL2 dramatically inhibited Ku70 and Ku80 recruitment and retentio","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Feb","modification":"2026-05-06T00:21:51.994Z","creation":"2019-08-04T07:05:39Z"},"accession":"S-EPMC5761340","cross_references":{"pubmed":["29179998"],"doi":["10.1016/j.canlet.2017.11.028"]}}