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MYC is downregulated by a mitochondrial checkpoint mechanism
Karolinska Institute, Sweden.
Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences.
Karolinska Institute, Sweden.
Karolinska Institute, Sweden.
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2017 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 8, no 52, p. 90225-90237Article in journal (Refereed) Published
Abstract [en]

The MYC proto-oncogene serves as a rheostat coupling mitogenic signaling with the activation of genes regulating growth, metabolism and mitochondrial biogenesis. Here we describe a novel link between mitochondria and MYC levels. Perturbation of mitochondrial function using a number of conventional and novel inhibitors resulted in the decreased expression of MYC mRNA. This decrease in MYC mRNA occurred concomitantly with an increase in the levels of tumor-suppressive miRNAs such as members of the let-7 family and miR-34a-5p. Knockdown of let-7 family or miR-34a-5p could partially restore MYC levels following mitochondria damage. We also identified let-7-dependent downregulation of the MYC mRNA chaperone, CRD-BP (coding region determinant-binding protein) as an additional control following mitochondria damage. Our data demonstrates the existence of a homeostasis mechanism whereby mitochondrial function controls MYC expression.

Place, publisher, year, edition, pages
IMPACT JOURNALS LLC , 2017. Vol. 8, no 52, p. 90225-90237
Keywords [en]
mitochondria; MYC; CRD-BP; let-7/miR-34a; cancer
National Category
Cell Biology
Identifiers
URN: urn:nbn:se:liu:diva-143740DOI: 10.18632/oncotarget.21653ISI: 000414097100067PubMedID: 29163823OAI: oai:DiVA.org:liu-143740DiVA, id: diva2:1166703
Note

Funding Agencies|Cancerfonden; Vetenskapsradet; Radiumhemmets forskningsfonder; Knut och Alice Wallenbergs Stiftelse; Barncancerfonden

Available from: 2017-12-15 Created: 2017-12-15 Last updated: 2018-01-26

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