{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Chu J"],"funding":["National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["1333-1348"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11445280"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["31(10)"],"pubmed_abstract":["The oncogenic potential of chromosome 8q22 copy number gain in liver cancer remains to be depicted. Here, we report that ZNF706, encoded by a gene mapped to chromosome 8q22, is a C2H2-type zinc finger protein. However, the biological function and mechanism of ZNF706 have been poorly investigated. Clinically, ZNF706 expression was elevated in hepatocellular carcinoma (HCC), and high ZNF706 expression was associated with unfavorable survival in HCC patients. Functional experiments revealed that ZNF706 knockdown inhibited HCC progression both in vitro and in vivo. RNA sequencing (RNA-seq) and chromatin immunoprecipitation-based deep sequencing (ChIP-seq) revealed that mechanistically, ZNF706 is a crucial ferroptosis regulator and that SLC7A11 is a critical target of ZNF706. In addition, ZNF70"],"journal":["Cell death and differentiation"],"pubmed_title":["A novel MYC-ZNF706-SLC7A11 regulatory circuit contributes to cancer progression and redox balance in human hepatocellular carcinoma."],"pmcid":["PMC11445280"],"funding_grant_id":["82103202","82173046"],"pubmed_authors":["Jiang Y","Jiang J","Xi W","Liu J","Fan X","Gao K","Bian K","Chu J","Zhang L","Yang A","Zhang R","Li M"],"additional_accession":[]},"is_claimable":false,"name":"A novel MYC-ZNF706-SLC7A11 regulatory circuit contributes to cancer progression and redox balance in human hepatocellular carcinoma.","description":"The oncogenic potential of chromosome 8q22 copy number gain in liver cancer remains to be depicted. Here, we report that ZNF706, encoded by a gene mapped to chromosome 8q22, is a C2H2-type zinc finger protein. However, the biological function and mechanism of ZNF706 have been poorly investigated. Clinically, ZNF706 expression was elevated in hepatocellular carcinoma (HCC), and high ZNF706 expression was associated with unfavorable survival in HCC patients. Functional experiments revealed that ZNF706 knockdown inhibited HCC progression both in vitro and in vivo. RNA sequencing (RNA-seq) and chromatin immunoprecipitation-based deep sequencing (ChIP-seq) revealed that mechanistically, ZNF706 is a crucial ferroptosis regulator and that SLC7A11 is a critical target of ZNF706. In addition, ZNF70","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Oct","modification":"2026-06-01T13:45:01.72Z","creation":"2025-04-04T12:53:22.024Z"},"accession":"S-EPMC11445280","cross_references":{"pubmed":["38862581"],"doi":["10.1038/s41418-024-01324-3"]}}