{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Guo Y"],"funding":["Program for Professor of Special Appointment (Young Eastern Scholar) at Shanghai Institutions of Higher Learning (to C-Y. L.).","National Natural Science Foundation of China"],"pagination":["4995"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9411202"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["13(1)"],"pubmed_abstract":["Dysregulation of Hippo pathway leads to hyperactivation of YAP-TEAD transcriptional complex in various cancers, including colorectal cancer (CRC). In this study, we observed that HHEX (Hematopoietically expressed homeobox) may enhance transcription activity of the YAP-TEAD complex. HHEX associates with and stabilizes the YAP-TEAD complex on the regulatory genomic loci to coregulate the expression of a group of YAP/TEAD target genes. Also, HHEX may indirectly regulate these target genes by controlling YAP/TAZ expression. Importantly, HHEX is required for the pro-tumorigenic effects of YAP during CRC progression. In response to serum stimulation, CK2 (Casein Kinase 2) phosphorylates HHEX and enhances its interaction with TEAD4. A CK2 inhibitor CX-4945 diminishes the interaction between HHEX "],"journal":["Nature communications"],"pubmed_title":["CK2-induced cooperation of HHEX with the YAP-TEAD4 complex promotes colorectal tumorigenesis."],"pmcid":["PMC9411202"],"funding_grant_id":["81874177","81974060","81873547","82073056"],"pubmed_authors":["Du P","Liu CY","Zhu Z","Guo Y","Huang Z","Cui L","Yu W","Hong W","Zhou Z"],"additional_accession":[]},"is_claimable":false,"name":"CK2-induced cooperation of HHEX with the YAP-TEAD4 complex promotes colorectal tumorigenesis.","description":"Dysregulation of Hippo pathway leads to hyperactivation of YAP-TEAD transcriptional complex in various cancers, including colorectal cancer (CRC). In this study, we observed that HHEX (Hematopoietically expressed homeobox) may enhance transcription activity of the YAP-TEAD complex. HHEX associates with and stabilizes the YAP-TEAD complex on the regulatory genomic loci to coregulate the expression of a group of YAP/TEAD target genes. Also, HHEX may indirectly regulate these target genes by controlling YAP/TAZ expression. Importantly, HHEX is required for the pro-tumorigenic effects of YAP during CRC progression. In response to serum stimulation, CK2 (Casein Kinase 2) phosphorylates HHEX and enhances its interaction with TEAD4. A CK2 inhibitor CX-4945 diminishes the interaction between HHEX ","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Aug","modification":"2026-05-28T01:11:47.488Z","creation":"2025-04-19T22:49:19.701Z"},"accession":"S-EPMC9411202","cross_references":{"pubmed":["36008411"],"doi":["10.1038/s41467-022-32674-6"]}}