<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Quijano-Rubio C</submitter><funding>Oncosuisse</funding><funding>Oncosuisse (OCS)</funding><pagination>341</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9338300</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>8(1)</volume><pubmed_abstract>CD95 (Fas/APO-1) is a multifunctional cell surface receptor with antithetic roles. First described to mediate cell death, interactions of CD95 with its natural ligand, CD95L, have also been described to induce tumor-promoting signaling leading to proliferation, invasion and stem cell maintenance, mainly in cancer cells that are resistant to CD95-mediated apoptosis. While activation of CD95-mediated apoptosis in cancer cells may not be clinically practicable due to toxicity, inhibition of tumor-promoting CD95 signaling holds therapeutic potential. In the present study, we characterized CD95 and CD95L expression in human glioma-initiating cells (GIC), a glioblastoma cell population with stem cell features, and investigated the consequences of CRISPR-Cas9-mediated CD95 or CD95L gene deletion.</pubmed_abstract><journal>Cell death discovery</journal><pubmed_title>CD95 gene deletion may reduce clonogenic growth and invasiveness of human glioblastoma cells in a CD95 ligand-independent manner.</pubmed_title><pmcid>PMC9338300</pmcid><funding_grant_id>KLS-3814-02-2016</funding_grant_id><pubmed_authors>Weller M</pubmed_authors><pubmed_authors>Quijano-Rubio C</pubmed_authors><pubmed_authors>Silginer M</pubmed_authors></additional><is_claimable>false</is_claimable><name>CD95 gene deletion may reduce clonogenic growth and invasiveness of human glioblastoma cells in a CD95 ligand-independent manner.</name><description>CD95 (Fas/APO-1) is a multifunctional cell surface receptor with antithetic roles. First described to mediate cell death, interactions of CD95 with its natural ligand, CD95L, have also been described to induce tumor-promoting signaling leading to proliferation, invasion and stem cell maintenance, mainly in cancer cells that are resistant to CD95-mediated apoptosis. While activation of CD95-mediated apoptosis in cancer cells may not be clinically practicable due to toxicity, inhibition of tumor-promoting CD95 signaling holds therapeutic potential. In the present study, we characterized CD95 and CD95L expression in human glioma-initiating cells (GIC), a glioblastoma cell population with stem cell features, and investigated the consequences of CRISPR-Cas9-mediated CD95 or CD95L gene deletion.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jul</publication><modification>2025-04-27T01:15:44.527Z</modification><creation>2025-04-06T18:08:43.716Z</creation></dates><accession>S-EPMC9338300</accession><cross_references><pubmed>35906203</pubmed><doi>10.1038/s41420-022-01133-y</doi></cross_references></HashMap>