{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Aoki K"],"funding":["Naito Foundation","MEXT | Japan Science and Technology Agency (JST)","Takeda Medical Research Foundation","Princess Takamatsu Cancer Research Fund","MEXT | Japan Science and Technology Agency"],"pagination":["408"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12095478"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["Homeobox transcription factors CDX1 and CDX2 (hereafter, CDX1/2) play key roles in determining the identity of intestinal epithelial cells and regulating their stem cell functions. However, the role of CDX1/2 in regulating colon cancer stemness and the underlying mechanisms are unclear. Here, we show that complete loss of Cdx1 or concurrent loss of Cdx1/2 increased the stemness and malignancy of intestinal tumors. Consistently, CDX1/2 reduced the expression of cancer stemness-related genes, including LGR5. CDX1/2 bound to the downstream region of the LGR5 transcription start site (TSS), a region where β-catenin also binds. Despite increased H3 acetylation and an open chromatin structure, CDX1/2 reduced the occupancy of DRB sensitivity-inducing factor (DSIF), RNA polymerase II-associated fa"],"journal":["Cell death & disease"],"pubmed_title":["CDX1 and CDX2 suppress colon cancer stemness by inhibiting β-catenin-facilitated formation of Pol II-DSIF-PAF1C complex."],"pmcid":["PMC12095478"],"funding_grant_id":["21K06946, 24650619, 24680091 and JPMJPR1181"],"pubmed_authors":["Nitta A","Aoki K","Igarashi A"],"additional_accession":[]},"is_claimable":false,"name":"CDX1 and CDX2 suppress colon cancer stemness by inhibiting β-catenin-facilitated formation of Pol II-DSIF-PAF1C complex.","description":"Homeobox transcription factors CDX1 and CDX2 (hereafter, CDX1/2) play key roles in determining the identity of intestinal epithelial cells and regulating their stem cell functions. However, the role of CDX1/2 in regulating colon cancer stemness and the underlying mechanisms are unclear. Here, we show that complete loss of Cdx1 or concurrent loss of Cdx1/2 increased the stemness and malignancy of intestinal tumors. Consistently, CDX1/2 reduced the expression of cancer stemness-related genes, including LGR5. CDX1/2 bound to the downstream region of the LGR5 transcription start site (TSS), a region where β-catenin also binds. Despite increased H3 acetylation and an open chromatin structure, CDX1/2 reduced the occupancy of DRB sensitivity-inducing factor (DSIF), RNA polymerase II-associated fa","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 May","modification":"2026-06-01T19:15:33.651Z","creation":"2026-05-21T03:08:48.229Z"},"accession":"S-EPMC12095478","cross_references":{"pubmed":["40399276"],"doi":["10.1038/s41419-025-07737-3"]}}