<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>19(1)</volume><submitter>Zheng L</submitter><pubmed_abstract>&lt;h4>Background&lt;/h4>We tried to elaborate the molecular mechanism of ETS-like transcription factor 4 (ELK4) affecting gastric cancer (GC) progression through M2 polarization of macrophages mediated by lysine-specific demethylase 5A (KDM5A)-Praja2 (PJA2)-kinase suppressor of ras 1 (KSR1) axis.&lt;h4>Methods&lt;/h4>GC expression dataset was obtained from GEO database, and the downstream regulatory mechanism of ELK4 was predicted. Tumor-associated macrophages (TAMs) were isolated from GC tissues. The interaction among ELK4, KDM5A, PJA2 and KSR1 was analyzed by dual luciferase reporter gene, ChIP and Co-IP assays. The stability of KSR1 protein was detected by cycloheximide (CHX) treatment. After TAMs were co-cultured with HGC-27 cells, HGC-27 cell biological processes were assessed through gain- and </pubmed_abstract><journal>Journal of translational medicine</journal><pagination>342</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8353876</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>ELK4 promotes the development of gastric cancer by inducing M2 polarization of macrophages through regulation of the KDM5A-PJA2-KSR1 axis.</pubmed_title><pmcid>PMC8353876</pmcid><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>Zheng L</pubmed_authors><pubmed_authors>Chen L</pubmed_authors><pubmed_authors>Gao L</pubmed_authors><pubmed_authors>Xu H</pubmed_authors><pubmed_authors>Di Y</pubmed_authors><pubmed_authors>Kang L</pubmed_authors></additional><is_claimable>false</is_claimable><name>ELK4 promotes the development of gastric cancer by inducing M2 polarization of macrophages through regulation of the KDM5A-PJA2-KSR1 axis.</name><description>&lt;h4>Background&lt;/h4>We tried to elaborate the molecular mechanism of ETS-like transcription factor 4 (ELK4) affecting gastric cancer (GC) progression through M2 polarization of macrophages mediated by lysine-specific demethylase 5A (KDM5A)-Praja2 (PJA2)-kinase suppressor of ras 1 (KSR1) axis.&lt;h4>Methods&lt;/h4>GC expression dataset was obtained from GEO database, and the downstream regulatory mechanism of ELK4 was predicted. Tumor-associated macrophages (TAMs) were isolated from GC tissues. The interaction among ELK4, KDM5A, PJA2 and KSR1 was analyzed by dual luciferase reporter gene, ChIP and Co-IP assays. The stability of KSR1 protein was detected by cycloheximide (CHX) treatment. After TAMs were co-cultured with HGC-27 cells, HGC-27 cell biological processes were assessed through gain- and </description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Aug</publication><modification>2026-05-08T20:54:07.342Z</modification><creation>2022-02-11T07:26:36.393Z</creation></dates><accession>S-EPMC8353876</accession><cross_references><pubmed>34372882</pubmed><doi>10.1186/s12967-021-02915-1</doi></cross_references></HashMap>