<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Cruz-Hernandez CD</submitter><funding>Consejo Nacional de Ciencia y Tecnología</funding><pagination>312</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7364616</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>20</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Prostate cancer (PCa) is the second cause of cancer related death in North American men. Androgens play an important role in its progression by regulating the expression of several genes including fusion ones that results from structural chromosome rearrangements. &lt;i>TMPRSS2&lt;/i>-&lt;i>ERG&lt;/i> is a fusion gene commonly observed in over 50% of PCa tumors, and its expression can be transcriptionally regulated by the androgen receptor (AR) given its androgen responsive elements. &lt;i>TMPRSS2&lt;/i>-&lt;i>ERG&lt;/i> could be involved in epithelial-mesenchymal transition (EMT) during tumor development. ERG has been reported as a key transcriptional factor in the AR-ERG-WNT network where five SFRP proteins, structurally similar to WNT ligands and considered to be WNT pathway antagonists, can</pubmed_abstract><journal>Cancer cell international</journal><pubmed_title>SFRP1 increases TMPRSS2-ERG expression promoting neoplastic features in prostate cancer in vitro and in vivo.</pubmed_title><pmcid>PMC7364616</pmcid><funding_grant_id>A1S26446</funding_grant_id><funding_grant_id>177687</funding_grant_id><pubmed_authors>Llaguno-Munive M</pubmed_authors><pubmed_authors>Langley E</pubmed_authors><pubmed_authors>Cruz-Hernandez CD</pubmed_authors><pubmed_authors>Losada-Garcia A</pubmed_authors><pubmed_authors>Camacho-Arroyo I</pubmed_authors><pubmed_authors>Cruz-Colin JL</pubmed_authors><pubmed_authors>Beltran-Anaya FO</pubmed_authors><pubmed_authors>Cortes-Ramirez SA</pubmed_authors><pubmed_authors>Cruz-Burgos M</pubmed_authors><pubmed_authors>Rodriguez-Dorantes M</pubmed_authors><pubmed_authors>Perez-Plasencia C</pubmed_authors><pubmed_authors>Albino-Sanchez ME</pubmed_authors><pubmed_authors>Gonzalez-Covarrubias V</pubmed_authors><pubmed_authors>Garcia-Lopez P</pubmed_authors></additional><is_claimable>false</is_claimable><name>SFRP1 increases TMPRSS2-ERG expression promoting neoplastic features in prostate cancer in vitro and in vivo.</name><description>&lt;h4>Background&lt;/h4>Prostate cancer (PCa) is the second cause of cancer related death in North American men. Androgens play an important role in its progression by regulating the expression of several genes including fusion ones that results from structural chromosome rearrangements. &lt;i>TMPRSS2&lt;/i>-&lt;i>ERG&lt;/i> is a fusion gene commonly observed in over 50% of PCa tumors, and its expression can be transcriptionally regulated by the androgen receptor (AR) given its androgen responsive elements. &lt;i>TMPRSS2&lt;/i>-&lt;i>ERG&lt;/i> could be involved in epithelial-mesenchymal transition (EMT) during tumor development. ERG has been reported as a key transcriptional factor in the AR-ERG-WNT network where five SFRP proteins, structurally similar to WNT ligands and considered to be WNT pathway antagonists, can</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020</publication><modification>2025-04-04T20:16:47.377Z</modification><creation>2025-04-04T20:16:47.377Z</creation></dates><accession>S-EPMC7364616</accession><cross_references><pubmed>32694934</pubmed><doi>10.1186/s12935-020-01333-5</doi></cross_references></HashMap>