<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Monteleone E</submitter><funding>Associazione Italiana per la Ricerca sul Cancro</funding><funding>Ministero dell'Istruzione, dell'Università e della Ricerca</funding><funding>Ministero dell’Istruzione, dell’Università e della Ricerca</funding><funding>Fondazione CRT</funding><funding>Truus and Gerrit van Riemsdijk Foundation, Liechtenstein</funding><funding>Compagnia di San Paolo</funding><pagination>E101</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6356433</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(1)</volume><pubmed_abstract>Breast cancer is a heterogeneous disease whose clinical management is very challenging. Although specific molecular features characterize breast cancer subtypes with different prognosis, the identification of specific markers predicting disease outcome within the single subtypes still lags behind. Both the non-canonical Wingless-type MMTV Integration site (WNT) and the Signal Transducer and Activator of Transcription (STAT)3 pathways are often constitutively activated in breast tumors, and both can induce the small GTPase Ras Homolog Family Member U &lt;i>RhoU&lt;/i>. Here we show that &lt;i>RhoU&lt;/i> transcription can be triggered by both canonical and non-canonical WNT ligands via the activation of c-JUN N-terminal kinase (JNK) and the recruitment of the Specificity Protein 1 (SP1) transcription f</pubmed_abstract><journal>Cancers</journal><pubmed_title>SP1 and STAT3 Functionally Synergize to Induce the &lt;i>RhoU&lt;/i> Small GTPase and a Subclass of Non-canonical WNT Responsive Genes Correlating with Poor Prognosis in Breast Cancer.</pubmed_title><pmcid>PMC6356433</pmcid><funding_grant_id>IG13009</funding_grant_id><funding_grant_id>VP1</funding_grant_id><funding_grant_id>IG16930</funding_grant_id><funding_grant_id>PRIN 2012 9JLHSY</funding_grant_id><funding_grant_id>VP</funding_grant_id><funding_grant_id>02_2012_0062</funding_grant_id><funding_grant_id>02_2012_0094</funding_grant_id><funding_grant_id>PRIN 2015 YYLBTR</funding_grant_id><pubmed_authors>Poli V</pubmed_authors><pubmed_authors>Avalle L</pubmed_authors><pubmed_authors>Molineris I</pubmed_authors><pubmed_authors>Provero P</pubmed_authors><pubmed_authors>Savino A</pubmed_authors><pubmed_authors>Orecchia V</pubmed_authors><pubmed_authors>Schiavone D</pubmed_authors><pubmed_authors>Corrieri P</pubmed_authors><pubmed_authors>Monteleone E</pubmed_authors><pubmed_authors>Moiso E</pubmed_authors></additional><is_claimable>false</is_claimable><name>SP1 and STAT3 Functionally Synergize to Induce the &lt;i>RhoU&lt;/i> Small GTPase and a Subclass of Non-canonical WNT Responsive Genes Correlating with Poor Prognosis in Breast Cancer.</name><description>Breast cancer is a heterogeneous disease whose clinical management is very challenging. Although specific molecular features characterize breast cancer subtypes with different prognosis, the identification of specific markers predicting disease outcome within the single subtypes still lags behind. Both the non-canonical Wingless-type MMTV Integration site (WNT) and the Signal Transducer and Activator of Transcription (STAT)3 pathways are often constitutively activated in breast tumors, and both can induce the small GTPase Ras Homolog Family Member U &lt;i>RhoU&lt;/i>. Here we show that &lt;i>RhoU&lt;/i> transcription can be triggered by both canonical and non-canonical WNT ligands via the activation of c-JUN N-terminal kinase (JNK) and the recruitment of the Specificity Protein 1 (SP1) transcription f</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019 Jan</publication><modification>2026-07-09T12:10:35.879Z</modification><creation>2019-03-26T22:47:54Z</creation></dates><accession>S-EPMC6356433</accession><cross_references><pubmed>30654518</pubmed><doi>10.3390/cancers11010101</doi></cross_references></HashMap>