<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>5</volume><submitter>Mombelli S</submitter><pubmed_abstract>Pro-inflammatory IL-17 cytokines were initially described for their pathogenic role in chronic inflammatory diseases and subsequent accumulating evidence indicated their involvement in carcinogenesis. In the present study we report that IL-17A and IL-17E receptors subunits mRNA expressions are upregulated in breast cancers versus normal samples. IL-17E, which is undetectable in most normal breast tissues tested, seems more expressed in some tumors. Investigation of the molecular signaling following stimulation of human breast cancer cell lines with IL-17A and IL-17E showed that both cytokines induced the phosphorylation of c-RAF, ERK1/2 and p70 S6 Kinase were involved in the proliferation and survival of tumor cells. Accordingly, IL-17A and IL-17E promoted resistance to Docetaxel and faile</pubmed_abstract><journal>Scientific reports</journal><pagination>11874</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4648389</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>IL-17A and its homologs IL-25/IL-17E recruit the c-RAF/S6 kinase pathway and the generation of pro-oncogenic LMW-E in breast cancer cells.</pubmed_title><pmcid>PMC4648389</pmcid><pubmed_authors>Eliaou JF</pubmed_authors><pubmed_authors>Bonnefoy N</pubmed_authors><pubmed_authors>Garbar C</pubmed_authors><pubmed_authors>Antonicelli F</pubmed_authors><pubmed_authors>Alberici G</pubmed_authors><pubmed_authors>Merrouche Y</pubmed_authors><pubmed_authors>Cochaud S</pubmed_authors><pubmed_authors>Laprevotte E</pubmed_authors><pubmed_authors>Bensussan A</pubmed_authors><pubmed_authors>Mombelli S</pubmed_authors><pubmed_authors>Bastid J</pubmed_authors><pubmed_authors>Giustiniani J</pubmed_authors></additional><is_claimable>false</is_claimable><name>IL-17A and its homologs IL-25/IL-17E recruit the c-RAF/S6 kinase pathway and the generation of pro-oncogenic LMW-E in breast cancer cells.</name><description>Pro-inflammatory IL-17 cytokines were initially described for their pathogenic role in chronic inflammatory diseases and subsequent accumulating evidence indicated their involvement in carcinogenesis. In the present study we report that IL-17A and IL-17E receptors subunits mRNA expressions are upregulated in breast cancers versus normal samples. IL-17E, which is undetectable in most normal breast tissues tested, seems more expressed in some tumors. Investigation of the molecular signaling following stimulation of human breast cancer cell lines with IL-17A and IL-17E showed that both cytokines induced the phosphorylation of c-RAF, ERK1/2 and p70 S6 Kinase were involved in the proliferation and survival of tumor cells. Accordingly, IL-17A and IL-17E promoted resistance to Docetaxel and faile</description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Jul</publication><modification>2026-05-05T10:44:05.85Z</modification><creation>2019-03-27T02:02:08Z</creation></dates><accession>S-EPMC4648389</accession><cross_references><pubmed>26154409</pubmed><doi>10.1038/srep11874</doi></cross_references></HashMap>