NAF-1 and mitoNEET are central to human breast cancer proliferation by maintaining mitochondrial homeostasis and promoting tumor growth

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dc.citation.journalTitlePNAS Early Editionen_US
dc.contributor.authorSohn, Yang-Sungen_US
dc.contributor.authorTamir, Sagien_US
dc.contributor.authorSong, Luhuaen_US
dc.contributor.authorMichaeli, Doriten_US
dc.contributor.authorMatouk, Imaden_US
dc.contributor.authorConlan, Andrea R.en_US
dc.contributor.authorHarir, Yaelen_US
dc.contributor.authorHolt, Sarah H.en_US
dc.contributor.authorShulaev, Vladimiren_US
dc.contributor.authorPaddock, Mark L.en_US
dc.contributor.authorHochberg, Abrahamen_US
dc.contributor.authorCabanchick, Ioav Z.en_US
dc.contributor.authorOnuchic, José N.en_US
dc.contributor.authorJennings, Patricia A.en_US
dc.contributor.authorNechushtai, Rachelen_US
dc.contributor.authorMittler, Ronen_US
dc.contributor.orgCenter for Theoretical Biological Physicsen_US
dc.date.accessioned2013-08-30T20:26:22Z
dc.date.available2013-08-30T20:26:22Z
dc.date.issued2013en_US
dc.description.abstractMitochondria are emerging as important players in the transformation process of cells, maintaining the biosynthetic and energetic capacities of cancer cells and serving as one of the primary sites of apoptosis and autophagy regulation. Although several avenues of cancer therapy have focused on mitochondria, progress in developing mitochondria-targeting anticancer drugs nonetheless has been slow, owing to the limited number of known mitochondrial target proteins that link metabolism with autophagy or cell death. Recent studies have demonstrated that two members of the newly discovered family of NEET proteins, NAF-1 (CISD2) and mitoNEET (mNT; CISD1), could play such a role in cancer cells. NAF-1 was shown to be a key player in regulating autophagy, and mNT was proposed to mediate iron and reactive oxygen homeostasis in mitochondria. Here we show that the protein levels of NAF-1 and mNT are elevated in human epithelial breast cancer cells, and that suppressing the level of these proteins using shRNA results in significantly reduced cell proliferation and tumor growth, decreased mitochondrial performance, uncontrolled accumulation of iron and reactive oxygen in mitochondria, and activation of autophagy. Our findings highlight NEET proteins as promising mitochondrial targets for cancer therapy.en_US
dc.embargo.termsnoneen_US
dc.identifier.citationSohn, Yang-Sung, Tamir, Sagi, Song, Luhua, et al.. "NAF-1 and mitoNEET are central to human breast cancer proliferation by maintaining mitochondrial homeostasis and promoting tumor growth." <i>PNAS Early Edition,</i> (2013) National Academy of Sciences: http://dx.doi.org/10.1073/pnas.1313198110.
dc.identifier.doihttp://dx.doi.org/10.1073/pnas.1313198110en_US
dc.identifier.urihttps://hdl.handle.net/1911/71866
dc.language.isoengen_US
dc.publisherNational Academy of Sciences
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
dc.subject.keywordCisd1en_US
dc.subject.keywordCisd2en_US
dc.subject.keywordMiner1en_US
dc.subject.keywordMCF7en_US
dc.subject.keywordMDA-MB-231en_US
dc.titleNAF-1 and mitoNEET are central to human breast cancer proliferation by maintaining mitochondrial homeostasis and promoting tumor growthen_US
dc.typeJournal articleen_US
dc.type.dcmiTexten_US
dc.type.publicationpublisher versionen_US
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