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In this study, we found that the patients of both myelodysplastic syndromes and chronic myeloid leukaemia with <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>1 overexpression had a higher risk in malignant myeloid progression. <jats:italic>In vitro<\/jats:italic> gene transfection studies showed that <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>1 inhibited cell myeloid and erythroid differentiation induced by 12\u2010O\u2010tetradecanoyl phorbol\u201013\u2010acetate (<jats:styled-content style=\"fixed-case\">TPA<\/jats:styled-content>) and histone deacetylase inhibitor sodium butyrate respectively. <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>1 also resisted apoptosis induced by arsenic trioxide. Moreover, the transcript levels of <jats:italic>Runx1<\/jats:italic> and <jats:italic>Pten<\/jats:italic> were down\u2010regulated in <jats:italic>Bmi1<\/jats:italic>\u2010transfected cells in company with histone deacetylation modification. By using chromatin immunoprecipitation (Ch<jats:styled-content style=\"fixed-case\">IP<\/jats:styled-content>) collaborated with secondary generation sequencing and verified by Ch<jats:styled-content style=\"fixed-case\">IP<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content>, we found that <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>1 directly bound to the promoter region of <jats:italic>Zmym3<\/jats:italic>, which encodes a component of histone deacetylase\u2010containing complexes. In addition, as one of the downstream target genes of this complex, <jats:italic>c\u2010fos<\/jats:italic> was activated with increasing histone acetylation when <jats:styled-content style=\"fixed-case\">ZMYM<\/jats:styled-content>3 was suppressed in the <jats:italic>Bmi1\u2010<\/jats:italic>transfected cells. These results suggested that <jats:styled-content style=\"fixed-case\">BMI<\/jats:styled-content>1 may reprogramme the histone acetylation profile in multiple genes through either indirect or direct binding effects which probably contributes to the malignant progression of myeloid progenitor cells.<\/jats:p>","DOI":"10.1111\/jcmm.12246","type":"journal-article","created":{"date-parts":[[2014,2,27]],"date-time":"2014-02-27T09:47:23Z","timestamp":1393494443000},"page":"1004-1017","source":"Crossref","is-referenced-by-count":13,"title":["BMI1 reprogrammes histone acetylation and enhances <i>c\u2010fos<\/i> pathway <i>via<\/i> directly binding to <i>Zmym3<\/i> in malignant myeloid progression"],"prefix":"10.1111","volume":"18","author":[{"given":"Hongjie","family":"Shen","sequence":"first","affiliation":[{"name":"Key Laboratory of Thrombosis and Hemostasis of Ministry of Health Jiangsu Institute of Hematology The First Affiliated Hospital of Soochow University Soochow 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