<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Gerlach K</submitter><funding>DFG</funding><funding>Interdisciplinary Center for Clinical Research</funding><funding>Medical Research Council</funding><funding>German Research Council</funding><funding>Collaborative Research Centers</funding><funding>Emerging Fields Initiative and the Ludwig Demling Center</funding><pagination>1893-1910</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10197880</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(12)</volume><pubmed_abstract>&lt;h4>Background and aims&lt;/h4>Colorectal cancer [CRC] is one of the most frequent malignancies, but the molecular mechanisms driving cancer growth are incompletely understood. We characterised the roles of the cytokine IL-9 and Th9 cells in regulating CRC development.&lt;h4>Methods&lt;/h4>CRC patient samples and samples from AOM/DSS treated mice were analysed for expression of IL-9, CD3, and PU.1 by FACS analysis and immunohistochemistry. IL-9 citrine reporter mice, IL-9 knockout mice, and PU.1 and GATA3 CD4-Cre conditional knockout mice were studied in the AOM/DSS model. DNA minicircles or hyper-IL-6 were used for overexpression of cytokines in vivo. Effects of IL-6 and IL-9 were determined in organoid and T cell cultures. Claudin2/3 expression was studied by western blotting and bacterial transl</pubmed_abstract><journal>Journal of Crohn's &amp; colitis</journal><pubmed_title>PU.1-driven Th9 Cells Promote Colorectal Cancer in Experimental Colitis Models Through Il-6 Effects in Intestinal Epithelial Cells.</pubmed_title><pmcid>PMC10197880</pmcid><funding_grant_id>CRC 1181/2-B02</funding_grant_id><funding_grant_id>MC_U105178805</funding_grant_id><funding_grant_id>GE3043/3-1 [434401404]</funding_grant_id><funding_grant_id>WE4656/2-2</funding_grant_id><pubmed_authors>Popp V</pubmed_authors><pubmed_authors>Atreya R</pubmed_authors><pubmed_authors>Dregelies T</pubmed_authors><pubmed_authors>Neurath MF</pubmed_authors><pubmed_authors>Gerlach K</pubmed_authors><pubmed_authors>Al-Saifi R</pubmed_authors><pubmed_authors>Rosenbauer F</pubmed_authors><pubmed_authors>Gonzalez Acera M</pubmed_authors><pubmed_authors>Fichtner-Feigl S</pubmed_authors><pubmed_authors>Vieth M</pubmed_authors><pubmed_authors>McKenzie ANJ</pubmed_authors><pubmed_authors>Wirtz S</pubmed_authors><pubmed_authors>Weigmann B</pubmed_authors></additional><is_claimable>false</is_claimable><name>PU.1-driven Th9 Cells Promote Colorectal Cancer in Experimental Colitis Models Through Il-6 Effects in Intestinal Epithelial Cells.</name><description>&lt;h4>Background and aims&lt;/h4>Colorectal cancer [CRC] is one of the most frequent malignancies, but the molecular mechanisms driving cancer growth are incompletely understood. We characterised the roles of the cytokine IL-9 and Th9 cells in regulating CRC development.&lt;h4>Methods&lt;/h4>CRC patient samples and samples from AOM/DSS treated mice were analysed for expression of IL-9, CD3, and PU.1 by FACS analysis and immunohistochemistry. IL-9 citrine reporter mice, IL-9 knockout mice, and PU.1 and GATA3 CD4-Cre conditional knockout mice were studied in the AOM/DSS model. DNA minicircles or hyper-IL-6 were used for overexpression of cytokines in vivo. Effects of IL-6 and IL-9 were determined in organoid and T cell cultures. Claudin2/3 expression was studied by western blotting and bacterial transl</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-04-21T22:46:22.617Z</modification><creation>2025-04-05T18:51:46.727Z</creation></dates><accession>S-EPMC10197880</accession><cross_references><pubmed>35793807</pubmed><doi>10.1093/ecco-jcc/jjac097</doi></cross_references></HashMap>