<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Sugita BM</submitter><funding>Georgetown University Center of Excellence in Regulatory Science and Innovation (CERSI)</funding><funding>Georgetown University Center of Excellence in Regulatory Science and Innovation</funding><funding>NCI NIH HHS</funding><pagination>2156</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9104497</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(9)</volume><pubmed_abstract>MiR-150-5p is frequently deregulated in cancer, with expression and mode of action varying according to the tumor type. Here, we investigated the expression levels and role of miR-150-5p in the aggressive breast cancer subtype triple-negative breast cancer (TNBC). MiR-150-5p expression levels were analyzed in tissue samples from 113 patients with invasive breast cancer (56 TNBC and 57 non-TNBC) and 41 adjacent non-tumor tissues (ANT). Overexpression of miR-150-5p was observed in tumor tissues compared with ANT tissues and in TNBC compared with non-TNBC tissues. MiR-150-5p expression levels were significantly associated with high tumor grades and the Caucasian ethnicity. Interestingly, high miR-150-5p levels were associated with prolonged overall survival. Manipulation of miR-150-5p expression in TNBC cells modulated cell proliferation, clonogenicity, migration, and drug resistance. Manipulation of miR-150-5p expression also resulted in altered expression of its mRNA targets, including epithelial-to-mesenchymal transition markers, &lt;i>MYB&lt;/i>, and members of the SRC pathway. These findings suggest that miR-150-5p is overexpressed in TNBC and contributes to the aggressiveness of TNBC cells in vitro.</pubmed_abstract><journal>Cancers</journal><pubmed_title>MiR-150-5p Overexpression in Triple-Negative Breast Cancer Contributes to the In Vitro Aggressiveness of This Breast Cancer Subtype.</pubmed_title><pmcid>PMC9104497</pmcid><funding_grant_id>U01FD004319</funding_grant_id><funding_grant_id>P30 CA051008</funding_grant_id><pubmed_authors>Fonseca AS</pubmed_authors><pubmed_authors>Kallakury B</pubmed_authors><pubmed_authors>Rodriguez Y</pubmed_authors><pubmed_authors>Cavalli IJ</pubmed_authors><pubmed_authors>Aneja R</pubmed_authors><pubmed_authors>Sugita BM</pubmed_authors><pubmed_authors>Nunes Souza E</pubmed_authors><pubmed_authors>Cavalli LR</pubmed_authors><pubmed_authors>Ribeiro EMSF</pubmed_authors></additional><is_claimable>false</is_claimable><name>MiR-150-5p Overexpression in Triple-Negative Breast Cancer Contributes to the In Vitro Aggressiveness of This Breast Cancer Subtype.</name><description>MiR-150-5p is frequently deregulated in cancer, with expression and mode of action varying according to the tumor type. Here, we investigated the expression levels and role of miR-150-5p in the aggressive breast cancer subtype triple-negative breast cancer (TNBC). MiR-150-5p expression levels were analyzed in tissue samples from 113 patients with invasive breast cancer (56 TNBC and 57 non-TNBC) and 41 adjacent non-tumor tissues (ANT). Overexpression of miR-150-5p was observed in tumor tissues compared with ANT tissues and in TNBC compared with non-TNBC tissues. MiR-150-5p expression levels were significantly associated with high tumor grades and the Caucasian ethnicity. Interestingly, high miR-150-5p levels were associated with prolonged overall survival. Manipulation of miR-150-5p expression in TNBC cells modulated cell proliferation, clonogenicity, migration, and drug resistance. Manipulation of miR-150-5p expression also resulted in altered expression of its mRNA targets, including epithelial-to-mesenchymal transition markers, &lt;i>MYB&lt;/i>, and members of the SRC pathway. These findings suggest that miR-150-5p is overexpressed in TNBC and contributes to the aggressiveness of TNBC cells in vitro.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Apr</publication><modification>2025-04-05T15:05:58.455Z</modification><creation>2025-04-05T15:05:58.455Z</creation></dates><accession>S-EPMC9104497</accession><cross_references><pubmed>35565284</pubmed><doi>10.3390/cancers14092156</doi></cross_references></HashMap>