<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Greene SB</submitter><funding>NCI NIH HHS</funding><pagination>606-18</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2818197</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>123(Pt 4)</volume><pubmed_abstract>In an effort to understand the potential role of microRNAs (miRNAs) in mammary-gland stem or progenitor cells, miRNA microarrays were performed on subpopulations of the mouse mammary epithelial cell (MEC) line COMMA-DbetaGeo. This cell line contains a heterogeneous subpopulation of progenitors characterized by the expression of stem cell antigen 1 (Sca-1; encoded by Ly6a). Microarray analysis indicated that the Sca-1 subpopulations have distinct miRNA expression profiles. Functional studies were performed on miR-205, which was highly expressed in the Sca-1-positive (Sca-1(+)) cells. When miR-205 was overexpressed in vitro, the COMMA-DbetaGeo cells underwent several significant morphological and molecular changes. miR-205 overexpression led to an expansion of the progenitor-cell population, decreased cell size and increased cellular proliferation. In addition, the colony-forming potential of the two Sca-1 subpopulations was increased. Target prediction for miR-205 indicated that it might regulate the expression of the tumor-suppressor protein PTEN. Overexpression studies using reporter constructs confirmed that PTEN expression is regulated by miR-205. In addition to PTEN, several other putative and previously validated miR-205 targets were identified by microarray analysis, including the previously reported miR-205 targets ZEB1 and ZEB2. Additionally, in normal mouse MECs, high expression of miR-205 was observed in stem-cell-enriched cell populations isolated by FACS using established cell-surface markers.</pubmed_abstract><journal>Journal of cell science</journal><pubmed_title>A putative role for microRNA-205 in mammary epithelial cell progenitors.</pubmed_title><pmcid>PMC2818197</pmcid><funding_grant_id>R37-CA16303-33</funding_grant_id><funding_grant_id>R37 CA016303</funding_grant_id><pubmed_authors>Greene SB</pubmed_authors><pubmed_authors>Gunaratne PH</pubmed_authors><pubmed_authors>Rosen JM</pubmed_authors><pubmed_authors>Hammond SM</pubmed_authors></additional><is_claimable>false</is_claimable><name>A putative role for microRNA-205 in mammary epithelial cell progenitors.</name><description>In an effort to understand the potential role of microRNAs (miRNAs) in mammary-gland stem or progenitor cells, miRNA microarrays were performed on subpopulations of the mouse mammary epithelial cell (MEC) line COMMA-DbetaGeo. This cell line contains a heterogeneous subpopulation of progenitors characterized by the expression of stem cell antigen 1 (Sca-1; encoded by Ly6a). Microarray analysis indicated that the Sca-1 subpopulations have distinct miRNA expression profiles. Functional studies were performed on miR-205, which was highly expressed in the Sca-1-positive (Sca-1(+)) cells. When miR-205 was overexpressed in vitro, the COMMA-DbetaGeo cells underwent several significant morphological and molecular changes. miR-205 overexpression led to an expansion of the progenitor-cell population, decreased cell size and increased cellular proliferation. In addition, the colony-forming potential of the two Sca-1 subpopulations was increased. Target prediction for miR-205 indicated that it might regulate the expression of the tumor-suppressor protein PTEN. Overexpression studies using reporter constructs confirmed that PTEN expression is regulated by miR-205. In addition to PTEN, several other putative and previously validated miR-205 targets were identified by microarray analysis, including the previously reported miR-205 targets ZEB1 and ZEB2. Additionally, in normal mouse MECs, high expression of miR-205 was observed in stem-cell-enriched cell populations isolated by FACS using established cell-surface markers.</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 Feb</publication><modification>2021-02-20T19:10:18Z</modification><creation>2019-03-27T00:28:24Z</creation></dates><accession>S-EPMC2818197</accession><cross_references><pubmed>20103531</pubmed><doi>10.1242/jcs.056812</doi></cross_references></HashMap>