{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ban GI"],"funding":["National Cancer Institute","NCI NIH HHS","NIAMS NIH HHS","NIH"],"pagination":["110187"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11233968"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(7)"],"pubmed_abstract":["Intratumoral heterogeneity is common in cancer, particularly in sarcomas like undifferentiated pleomorphic sarcoma (UPS), where individual cells demonstrate a high degree of cytogenic diversity. Previous studies showed that a small subset of cells within UPS, known as the metastatic clone (MC), as responsible for metastasis. Using a CRISPR-based genomic screen <i>in-vivo</i>, we identified the COMPASS complex member <i>Setd1a</i> as a key regulator maintaining the metastatic phenotype of the MC in murine UPS. Depletion of <i>Setd1a</i> inhibited metastasis development in the MC. Transcriptome and chromatin sequencing revealed COMPASS complex target genes in UPS, such as <i>Cxcl10</i>, downregulated in the MC. Deleting <i>Cxcl10</i> in non-MC cells increased their metastatic potential. Trea"],"journal":["iScience"],"pubmed_title":["The COMPASS complex maintains the metastatic capacity imparted by a subpopulation of cells in UPS."],"pmcid":["PMC11233968"],"funding_grant_id":["R35 CA197616","R00 AR077685","R01 CA183811","R01 CA251407","2R35 CA197616"],"pubmed_authors":["Nakagawa M","Browne M","Alman BA","Nadesan P","Ishikawa K","Guardino N","Tang J","Kirsch DG","Diao Y","Shimada E","Ou J","Martin JT","Puviindran V","Xiang Y","Ban GI","Wallace A"],"additional_accession":[]},"is_claimable":false,"name":"The COMPASS complex maintains the metastatic capacity imparted by a subpopulation of cells in UPS.","description":"Intratumoral heterogeneity is common in cancer, particularly in sarcomas like undifferentiated pleomorphic sarcoma (UPS), where individual cells demonstrate a high degree of cytogenic diversity. Previous studies showed that a small subset of cells within UPS, known as the metastatic clone (MC), as responsible for metastasis. Using a CRISPR-based genomic screen <i>in-vivo</i>, we identified the COMPASS complex member <i>Setd1a</i> as a key regulator maintaining the metastatic phenotype of the MC in murine UPS. Depletion of <i>Setd1a</i> inhibited metastasis development in the MC. Transcriptome and chromatin sequencing revealed COMPASS complex target genes in UPS, such as <i>Cxcl10</i>, downregulated in the MC. Deleting <i>Cxcl10</i> in non-MC cells increased their metastatic potential. Trea","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2026-06-01T07:03:28.078Z","creation":"2024-11-09T15:17:09.164Z"},"accession":"S-EPMC11233968","cross_references":{"pubmed":["38989451"],"doi":["10.1016/j.isci.2024.110187"]}}