{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ai L"],"funding":["NCI NIH HHS"],"pagination":["4875-87"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC4329918"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["74(17)"],"pubmed_abstract":["TRIM29 (ATDC) exhibits a contextual function in cancer, but seems to exert a tumor-suppressor role in breast cancer. Here, we show that TRIM29 is often silenced in primary breast tumors and cultured tumor cells as a result of aberrant gene hypermethylation. RNAi-mediated silencing of TRIM29 in breast tumor cells increased their motility, invasiveness, and proliferation in a manner associated with increased expression of mesenchymal markers (N-cadherin and vimentin), decreased expression of epithelial markers (E-cadherin and EpCAM), and increased expression and activity of the oncogenic transcription factor TWIST1, an important driver of the epithelial-mesenchymal transition (EMT). Functional investigations revealed an inverse relationship in the expression of TRIM29 and TWIST1, suggesting "],"journal":["Cancer research"],"pubmed_title":["TRIM29 suppresses TWIST1 and invasive breast cancer behavior."],"pmcid":["PMC4329918"],"funding_grant_id":["R03 CA143980","1R03CA143980","R01 CA155390","P30 CA076292"],"pubmed_authors":["Kim WJ","Pardo CE","Alpay M","Tang M","Kladde MP","Heldermon CD","May WS","Hatakeyama S","Ai L","Siegel EM","Brown KD"],"additional_accession":[]},"is_claimable":false,"name":"TRIM29 suppresses TWIST1 and invasive breast cancer behavior.","description":"TRIM29 (ATDC) exhibits a contextual function in cancer, but seems to exert a tumor-suppressor role in breast cancer. Here, we show that TRIM29 is often silenced in primary breast tumors and cultured tumor cells as a result of aberrant gene hypermethylation. RNAi-mediated silencing of TRIM29 in breast tumor cells increased their motility, invasiveness, and proliferation in a manner associated with increased expression of mesenchymal markers (N-cadherin and vimentin), decreased expression of epithelial markers (E-cadherin and EpCAM), and increased expression and activity of the oncogenic transcription factor TWIST1, an important driver of the epithelial-mesenchymal transition (EMT). Functional investigations revealed an inverse relationship in the expression of TRIM29 and TWIST1, suggesting ","dates":{"release":"2014-01-01T00:00:00Z","publication":"2014 Sep","modification":"2025-04-04T14:39:52.024Z","creation":"2019-03-27T01:45:17Z"},"accession":"S-EPMC4329918","cross_references":{"pubmed":["24950909"],"doi":["10.1158/0008-5472.can-13-3579","10.1158/0008-5472.CAN-13-3579"]}}