<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bhatt AB</submitter><funding>NCI</funding><funding>NCI NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>101046</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8020482</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>14(6)</volume><pubmed_abstract>The epithelial to mesenchymal transition (EMT) is characterized by a loss of cell polarity, a decrease in the epithelial cell marker E-cadherin, and an increase in mesenchymal markers including the zinc-finger E-box binding homeobox (ZEB1). The EMT is also associated with an increase in cell migration and anchorage-independent growth. Induction of a reversal of the EMT, a mesenchymal to epithelial transition (MET), is an emerging strategy being explored to attenuate the metastatic potential of aggressive cancer types, such as triple-negative breast cancers (TNBCs) and tamoxifen-resistant (TAMR) ER-positive breast cancers, which have a mesenchymal phenotype. Patients with these aggressive cancers have poor prognoses, quick relapse, and resistance to most chemotherapeutic drugs. Overexpressi</pubmed_abstract><journal>Translational oncology</journal><pubmed_title>Diverse and converging roles of ERK1/2 and ERK5 pathways on mesenchymal to epithelial transition in breast cancer.</pubmed_title><pmcid>PMC8020482</pmcid><funding_grant_id>R15 CA176496</funding_grant_id><funding_grant_id>U54 GM104940</funding_grant_id><pubmed_authors>Lexner E</pubmed_authors><pubmed_authors>Miele L</pubmed_authors><pubmed_authors>Burow ME</pubmed_authors><pubmed_authors>Flaherty PT</pubmed_authors><pubmed_authors>Ucar DA</pubmed_authors><pubmed_authors>Matossian MD</pubmed_authors><pubmed_authors>Bhatt AB</pubmed_authors><pubmed_authors>Wright TD</pubmed_authors><pubmed_authors>Chakrabarty S</pubmed_authors><pubmed_authors>Barnes V</pubmed_authors><pubmed_authors>Cavanaugh JE</pubmed_authors></additional><is_claimable>false</is_claimable><name>Diverse and converging roles of ERK1/2 and ERK5 pathways on mesenchymal to epithelial transition in breast cancer.</name><description>The epithelial to mesenchymal transition (EMT) is characterized by a loss of cell polarity, a decrease in the epithelial cell marker E-cadherin, and an increase in mesenchymal markers including the zinc-finger E-box binding homeobox (ZEB1). The EMT is also associated with an increase in cell migration and anchorage-independent growth. Induction of a reversal of the EMT, a mesenchymal to epithelial transition (MET), is an emerging strategy being explored to attenuate the metastatic potential of aggressive cancer types, such as triple-negative breast cancers (TNBCs) and tamoxifen-resistant (TAMR) ER-positive breast cancers, which have a mesenchymal phenotype. Patients with these aggressive cancers have poor prognoses, quick relapse, and resistance to most chemotherapeutic drugs. Overexpressi</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Jun</publication><modification>2026-05-10T02:40:55.99Z</modification><creation>2022-02-09T12:49:17.433Z</creation></dates><accession>S-EPMC8020482</accession><cross_references><pubmed>33761370</pubmed><doi>10.1016/j.tranon.2021.101046</doi></cross_references></HashMap>