{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,26]],"date-time":"2026-02-26T14:55:12Z","timestamp":1772117712387,"version":"3.50.1"},"reference-count":46,"publisher":"Wiley","license":[{"start":{"date-parts":[[2024,3,8]],"date-time":"2024-03-08T00:00:00Z","timestamp":1709856000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100016131","name":"Howat Foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100016131","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100010269","name":"Wellcome Trust","doi-asserted-by":"publisher","award":["105614\/Z\/14\/Z"],"award-info":[{"award-number":["105614\/Z\/14\/Z"]}],"id":[{"id":"10.13039\/100010269","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000582","name":"Carnegie Trust for the Universities of Scotland","doi-asserted-by":"publisher","award":["PHD007721"],"award-info":[{"award-number":["PHD007721"]}],"id":[{"id":"10.13039\/501100000582","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100009187","name":"Medical Research Foundation","doi-asserted-by":"publisher","award":["18048"],"award-info":[{"award-number":["18048"]}],"id":[{"id":"10.13039\/501100009187","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["febs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Molecular Oncology"],"abstract":"<jats:p>\n                    Acute myeloid leukaemia (AML) is a clonal haematological malignancy affecting the myeloid lineage, with generally poor patient outcomes owing to the lack of targeted therapies. The histone lysine demethylase 4A (KDM4A) has been established as a novel therapeutic target in AML, due to its selective oncogenic role within leukaemic cells. We identify that the transcription factor nuclear factor of activated T cells 2 (\n                    <jats:italic>NFATC2<\/jats:italic>\n                    ) is a novel binding and transcriptional target of KDM4A in the human AML THP\u20101 cell line. Furthermore, cytogenetically diverse AML cell lines, including THP\u20101, were dependent on\n                    <jats:italic>NFATC2<\/jats:italic>\n                    for colony formation\n                    <jats:italic>in vitro<\/jats:italic>\n                    , highlighting a putative novel mechanism of AML oncogenesis. Our study demonstrates that\n                    <jats:italic>NFATC2<\/jats:italic>\n                    maintenance of cell cycle progression in human AML cells was driven primarily by\n                    <jats:italic>CCND1<\/jats:italic>\n                    . Through RNA sequencing (RNA\u2010seq) and chromatin immunoprecipitation sequencing (ChIP\u2010seq), NFATc2 was shown to bind to the promoter region of genes involved in oxidative phosphorylation and subsequently regulate their gene expression in THP\u20101 cells. Furthermore, our data show that\n                    <jats:italic>NFATC2<\/jats:italic>\n                    shares transcriptional targets with the transcription factor c\u2010MYC, with\n                    <jats:italic>MYC<\/jats:italic>\n                    knockdown phenocopying\n                    <jats:italic>NFATC2<\/jats:italic>\n                    knockdown. These data suggest a newly identified co\u2010ordinated role for\n                    <jats:italic>NFATC2<\/jats:italic>\n                    and\n                    <jats:italic>MYC<\/jats:italic>\n                    in the maintenance of THP\u20101 cell function, indicative of a potential means of therapeutic targeting in human AML.\n                  <\/jats:p>","DOI":"10.1002\/1878-0261.13630","type":"journal-article","created":{"date-parts":[[2024,3,8]],"date-time":"2024-03-08T23:02:21Z","timestamp":1709938941000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["The\n                    <i>MYC\u2013NFATC2<\/i>\n                    axis maintains the cell cycle and mitochondrial function in acute myeloid leukaemia cells"],"prefix":"10.1002","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7131-1533","authenticated-orcid":false,"given":"Shaun 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