<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sheng X</submitter><funding>Science and Technology Commission of Shanghai Municipality</funding><funding>Multidisciplinary Cross Research Foundation of Shanghai Jiao Tong University</funding><funding>Shanghai Collaborative Innovation Center for Translational Medicine</funding><funding>Shanghai Natural Science Foundation</funding><funding>National Natural Science Foundation of China</funding><funding>the Shanghai Rising Stars of Medical Talent Youth Development Program for Outstanding Youth Medical Talents</funding><funding>Clinical Research Plan of SHDC</funding><funding>Shanghai Municipal Key Clinical Specialty</funding><funding>the Nurturing Fund of Renji Hospital</funding><pagination>205</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8220716</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>40(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Triple negative breast cancer (TNBC) is a subtype of breast cancer with poor prognosis and lack of effective treatment target. Here we screened differentially expressed lncRNAs through bioinformatics analysis and identified CARMN as a downregulated lncRNA which is lowest expressed in TNBC. We aimed to identify the potential role and molecular mechanisms of CARMN in TNBC.&lt;h4>Methods&lt;/h4>Predictive value of CARMN was explored in breast cancer cohorts. TNBC cell lines with CARMN overexpression or CARMN silence and were used for in vitro and in vivo experiments. RNA-seq of CARMN overexpressed cells was performed for exploring downstream of CARMN.&lt;h4>Results&lt;/h4>CARMN is downregulated at different phase of malignant transformation of breast tissue. CARMN can predict both bett</pubmed_abstract><journal>Journal of experimental &amp; clinical cancer research : CR</journal><pubmed_title>LncRNA CARMN overexpression promotes prognosis and chemosensitivity of triple negative breast cancer via acting as miR143-3p host gene and inhibiting DNA replication.</pubmed_title><pmcid>PMC8220716</pmcid><funding_grant_id>ZH2018QNA42</funding_grant_id><funding_grant_id>PYMDT-002</funding_grant_id><funding_grant_id>2018-16</funding_grant_id><funding_grant_id>82002777</funding_grant_id><funding_grant_id>YG2019QNA26</funding_grant_id><funding_grant_id>19ZR1431100</funding_grant_id><funding_grant_id>TM201908</funding_grant_id><funding_grant_id>SHDC2020CR3003A</funding_grant_id><funding_grant_id>20DZ2201600</funding_grant_id><pubmed_authors>Sheng X</pubmed_authors><pubmed_authors>Zhou L</pubmed_authors><pubmed_authors>Yin W</pubmed_authors><pubmed_authors>Lu J</pubmed_authors><pubmed_authors>Xu S</pubmed_authors><pubmed_authors>Du Y</pubmed_authors><pubmed_authors>Lin Y</pubmed_authors><pubmed_authors>Sha R</pubmed_authors><pubmed_authors>Peng J</pubmed_authors><pubmed_authors>Yang F</pubmed_authors><pubmed_authors>Wu Y</pubmed_authors><pubmed_authors>Dai H</pubmed_authors></additional><is_claimable>false</is_claimable><name>LncRNA CARMN overexpression promotes prognosis and chemosensitivity of triple negative breast cancer via acting as miR143-3p host gene and inhibiting DNA replication.</name><description>&lt;h4>Background&lt;/h4>Triple negative breast cancer (TNBC) is a subtype of breast cancer with poor prognosis and lack of effective treatment target. Here we screened differentially expressed lncRNAs through bioinformatics analysis and identified CARMN as a downregulated lncRNA which is lowest expressed in TNBC. We aimed to identify the potential role and molecular mechanisms of CARMN in TNBC.&lt;h4>Methods&lt;/h4>Predictive value of CARMN was explored in breast cancer cohorts. TNBC cell lines with CARMN overexpression or CARMN silence and were used for in vitro and in vivo experiments. RNA-seq of CARMN overexpressed cells was performed for exploring downstream of CARMN.&lt;h4>Results&lt;/h4>CARMN is downregulated at different phase of malignant transformation of breast tissue. CARMN can predict both bett</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jun</publication><modification>2026-05-09T09:03:48.647Z</modification><creation>2022-02-10T16:44:38.717Z</creation></dates><accession>S-EPMC8220716</accession><cross_references><pubmed>34162418</pubmed><doi>10.1186/s13046-021-02015-4</doi></cross_references></HashMap>