<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Ai L</submitter><funding>NCI NIH HHS</funding><pagination>4875-87</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4329918</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>74(17)</volume><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 </pubmed_abstract><journal>Cancer research</journal><pubmed_title>TRIM29 suppresses TWIST1 and invasive breast cancer behavior.</pubmed_title><pmcid>PMC4329918</pmcid><funding_grant_id>R03 CA143980</funding_grant_id><funding_grant_id>1R03CA143980</funding_grant_id><funding_grant_id>R01 CA155390</funding_grant_id><funding_grant_id>P30 CA076292</funding_grant_id><pubmed_authors>Kim WJ</pubmed_authors><pubmed_authors>Pardo CE</pubmed_authors><pubmed_authors>Alpay M</pubmed_authors><pubmed_authors>Tang M</pubmed_authors><pubmed_authors>Kladde MP</pubmed_authors><pubmed_authors>Heldermon CD</pubmed_authors><pubmed_authors>May WS</pubmed_authors><pubmed_authors>Hatakeyama S</pubmed_authors><pubmed_authors>Ai L</pubmed_authors><pubmed_authors>Siegel EM</pubmed_authors><pubmed_authors>Brown KD</pubmed_authors></additional><is_claimable>false</is_claimable><name>TRIM29 suppresses TWIST1 and invasive breast cancer behavior.</name><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 </description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Sep</publication><modification>2025-04-04T14:39:52.024Z</modification><creation>2019-03-27T01:45:17Z</creation></dates><accession>S-EPMC4329918</accession><cross_references><pubmed>24950909</pubmed><doi>10.1158/0008-5472.can-13-3579</doi><doi>10.1158/0008-5472.CAN-13-3579</doi></cross_references></HashMap>