{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Frohlich J"],"funding":["Deutsche Forschungsgemeinschaft","Albert-Ludwigs-Universität Freiburg im Breisgau"],"pagination":["287"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9822887"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Unrestrained transcriptional activity of β-CATENIN and its binding partner TCF7L2 frequently underlies colorectal tumor initiation and is considered an obligatory oncogenic driver throughout intestinal carcinogenesis. Yet, the TCF7L2 gene carries inactivating mutations in about 10% of colorectal tumors and is non-essential in colorectal cancer (CRC) cell lines. To determine whether CRC cells acquire TCF7L2-independence through cancer-specific compensation by other T-cell factor (TCF)/lymphoid enhancer-binding factor (LEF) family members, or rather lose addiction to β-CATENIN/TCF7L2-driven gene expression altogether, we generated multiple CRC cell lines entirely negative for TCF/LEF or β-CATENIN expression. Survival of these cells and the ability to propagate them demonstrate their complete"],"journal":["Scientific reports"],"pubmed_title":["Transcriptional activity mediated by β-CATENIN and TCF/LEF family members is completely dispensable for survival and propagation of multiple human colorectal cancer cell lines."],"pmcid":["PMC9822887"],"funding_grant_id":["322977937/GRK2344"],"pubmed_authors":["Rose K","Frohlich J","Hecht A"],"additional_accession":[]},"is_claimable":false,"name":"Transcriptional activity mediated by β-CATENIN and TCF/LEF family members is completely dispensable for survival and propagation of multiple human colorectal cancer cell lines.","description":"Unrestrained transcriptional activity of β-CATENIN and its binding partner TCF7L2 frequently underlies colorectal tumor initiation and is considered an obligatory oncogenic driver throughout intestinal carcinogenesis. Yet, the TCF7L2 gene carries inactivating mutations in about 10% of colorectal tumors and is non-essential in colorectal cancer (CRC) cell lines. To determine whether CRC cells acquire TCF7L2-independence through cancer-specific compensation by other T-cell factor (TCF)/lymphoid enhancer-binding factor (LEF) family members, or rather lose addiction to β-CATENIN/TCF7L2-driven gene expression altogether, we generated multiple CRC cell lines entirely negative for TCF/LEF or β-CATENIN expression. Survival of these cells and the ability to propagate them demonstrate their complete","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-05-29T16:22:37.691Z","creation":"2025-04-04T20:32:42.278Z"},"accession":"S-EPMC9822887","cross_references":{"pubmed":["36609428"],"doi":["10.1038/s41598-022-27261-0"]}}