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Cre-mediated deletion of E4F1 resulted in the death of HS cells and tumor regression in vivo and extended the lifespan of recipient animals. In murine and human HS cell lines, E4F1 inactivation resulted in mitochondrial defects and increased production of reactive oxygen species (ROS) that triggered massive cell death. Notably, these defects of E4F1 depletion were observed in HS cells but not healthy primary macrophages. Short hairpin RNA\u2013mediated depletion of E4F1 induced mitochondrial defects and ROS-mediated death in several human myeloid leukemia cell lines. E4F1 protein is overexpressed in a large subset of human acute myeloid leukemia samples. Together, these data reveal a role for E4F1 in the survival of myeloid leukemic cells and support the notion that targeting E4F1 activities might have therapeutic interest.<\/jats:p>","DOI":"10.1084\/jem.20101995","type":"journal-article","created":{"date-parts":[[2011,6,28]],"date-time":"2011-06-28T08:49:20Z","timestamp":1309250960000},"page":"1403-1417","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":32,"title":["E4F1 deficiency results in oxidative stress\u2013mediated cell death of leukemic cells"],"prefix":"10.1084","volume":"208","author":[{"given":"Elodie","family":"Hatchi","sequence":"first","affiliation":[{"name":"Institut de G\u00e9n\u00e9tique Mol\u00e9culaire de Montpellier, Centre National de la Recherche Scientifique Unit\u00e9 Mixte de Recherche 5535, Institut F\u00e9d\u00e9ratif de Recherche 122, Universit\u00e9 de Montpellier, Montpellier 34293, France 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