<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Guo X</submitter><funding>Taishan Scholarship Young Expert Program</funding><funding>Natural Science Foundation of Shandong Province</funding><funding>National Natural Science Foundation of China</funding><funding>Youth Innovation of Colleges and Universities of Shandong Province of China</funding><funding>Key Research and Development Program of Shandong Province</funding><funding>National Key Research and Development Program of China</funding><pagination>e70128</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11632201</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>30(12)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>The presence of glioma stem cells (GSCs) and the occurrence of mesenchymal phenotype transition contribute to the miserable prognosis of glioblastoma (GBM). Cellular communication network factor 1 (CCN1) is upregulated within various malignancies and associated with cancer development and progression, while the implications of CCN1 in the phenotype transition and tumorigenicity of GSCs remain unclear.&lt;h4>Methods&lt;/h4>Data for bioinformatic analysis were obtained from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) databases. A range of primary GBM and GSC cell models were then used to demonstrate the regulatory role of CCN1 via the phenotype validation, tumor sphere formation assays, extreme limiting dilution assays (ELDA), and transwell assays. To s</pubmed_abstract><journal>CNS neuroscience &amp; therapeutics</journal><pubmed_title>CCN1 Promotes Mesenchymal Phenotype Transition Through Activating NF-κB Signaling Pathway Regulated by S100A8 in Glioma Stem Cells.</pubmed_title><pmcid>PMC11632201</pmcid><funding_grant_id>ZR2023MH036</funding_grant_id><funding_grant_id>2023YFC2413004</funding_grant_id><funding_grant_id>2022YFC2406404</funding_grant_id><funding_grant_id>82272413</funding_grant_id><funding_grant_id>2023KJ023</funding_grant_id><funding_grant_id>tsqn201909174</funding_grant_id><funding_grant_id>2021ZLGX02</funding_grant_id><pubmed_authors>Tian F</pubmed_authors><pubmed_authors>Fan Y</pubmed_authors><pubmed_authors>Guo X</pubmed_authors><pubmed_authors>Wang C</pubmed_authors><pubmed_authors>Gao Z</pubmed_authors><pubmed_authors>Xu S</pubmed_authors><pubmed_authors>Guo S</pubmed_authors></additional><is_claimable>false</is_claimable><name>CCN1 Promotes Mesenchymal Phenotype Transition Through Activating NF-κB Signaling Pathway Regulated by S100A8 in Glioma Stem Cells.</name><description>&lt;h4>Background&lt;/h4>The presence of glioma stem cells (GSCs) and the occurrence of mesenchymal phenotype transition contribute to the miserable prognosis of glioblastoma (GBM). Cellular communication network factor 1 (CCN1) is upregulated within various malignancies and associated with cancer development and progression, while the implications of CCN1 in the phenotype transition and tumorigenicity of GSCs remain unclear.&lt;h4>Methods&lt;/h4>Data for bioinformatic analysis were obtained from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA) databases. A range of primary GBM and GSC cell models were then used to demonstrate the regulatory role of CCN1 via the phenotype validation, tumor sphere formation assays, extreme limiting dilution assays (ELDA), and transwell assays. To s</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2025-04-22T13:09:29.434Z</modification><creation>2025-04-06T00:35:46.233Z</creation></dates><accession>S-EPMC11632201</accession><cross_references><pubmed>39659236</pubmed><doi>10.1111/cns.70128</doi></cross_references></HashMap>