<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Kim DS</submitter><funding>NIDDK NIH HHS</funding><funding>Susan G. Komen</funding><funding>U.S. Department of Defense -BCRP</funding><funding>NCI NIH HHS</funding><funding>Cancer Prevention and Research Institute of Texas</funding><funding>NIH HHS</funding><pagination>1623-1635</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9633386</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20(11)</volume><pubmed_abstract>Long noncoding RNAs have been implicated in many of the hallmarks of cancer. Herein, we found that the expression of lncRNA152 (lnc152; a.k.a. DRAIC), which we annotated previously, is highly upregulated in luminal breast cancer (LBC) and downregulated in triple-negative breast cancer (TNBC). Knockdown of lnc152 promotes cell migration and invasion in LBC cell lines. In contrast, ectopic expression of lnc152 inhibits growth, migration, invasion, and angiogenesis in TNBC cell lines. In mice, lnc152 inhibited the growth of TNBC cell xenografts, as well as metastasis of TNBC cells in an intracardiac injection model. Transcriptome analysis of the xenografts indicated that lnc152 downregulates genes controlling angiogenesis. Using pull down assays followed by LC/MS-MS, we identified RBM47, a kn</pubmed_abstract><journal>Molecular cancer research : MCR</journal><pubmed_title>Functional Characterization of lncRNA152 as an Angiogenesis-Inhibiting Tumor Suppressor in Triple-Negative Breast Cancers.</pubmed_title><pmcid>PMC9633386</pmcid><funding_grant_id>S10 OD021684</funding_grant_id><funding_grant_id>RP190235</funding_grant_id><funding_grant_id>RP160318</funding_grant_id><funding_grant_id>R01 DK069710</funding_grant_id><funding_grant_id>RP130607</funding_grant_id><funding_grant_id>PDF230441</funding_grant_id><funding_grant_id>BC134066</funding_grant_id><funding_grant_id>P30 CA142543</funding_grant_id><pubmed_authors>Camacho CV</pubmed_authors><pubmed_authors>Kim DS</pubmed_authors><pubmed_authors>Kraus WL</pubmed_authors><pubmed_authors>Kim K</pubmed_authors><pubmed_authors>Hou TY</pubmed_authors><pubmed_authors>Nandu T</pubmed_authors><pubmed_authors>Gadad SS</pubmed_authors><pubmed_authors>Malladi S</pubmed_authors><pubmed_authors>Setlem R</pubmed_authors></additional><is_claimable>false</is_claimable><name>Functional Characterization of lncRNA152 as an Angiogenesis-Inhibiting Tumor Suppressor in Triple-Negative Breast Cancers.</name><description>Long noncoding RNAs have been implicated in many of the hallmarks of cancer. Herein, we found that the expression of lncRNA152 (lnc152; a.k.a. DRAIC), which we annotated previously, is highly upregulated in luminal breast cancer (LBC) and downregulated in triple-negative breast cancer (TNBC). Knockdown of lnc152 promotes cell migration and invasion in LBC cell lines. In contrast, ectopic expression of lnc152 inhibits growth, migration, invasion, and angiogenesis in TNBC cell lines. In mice, lnc152 inhibited the growth of TNBC cell xenografts, as well as metastasis of TNBC cells in an intracardiac injection model. Transcriptome analysis of the xenografts indicated that lnc152 downregulates genes controlling angiogenesis. Using pull down assays followed by LC/MS-MS, we identified RBM47, a kn</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2026-05-27T10:53:55.889Z</modification><creation>2024-11-20T02:13:49.764Z</creation></dates><accession>S-EPMC9633386</accession><cross_references><pubmed>35997635</pubmed><doi>10.1158/1541-7786.mcr-22-0123</doi><doi>10.1158/1541-7786.MCR-22-0123</doi></cross_references></HashMap>