AMPK and PFKFB3 mediate glycolysis and survival in response to mitophagy during mitotic arrest View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2015-10

AUTHORS

Elena Doménech, Carolina Maestre, Lorena Esteban-Martínez, David Partida, Rosa Pascual, Gonzalo Fernández-Miranda, Esther Seco, Ramón Campos-Olivas, Manuel Pérez, Diego Megias, Katherine Allen, Miguel López, Asish K. Saha, Guillermo Velasco, Eduardo Rial, Raúl Méndez, Patricia Boya, María Salazar-Roa, Marcos Malumbres

ABSTRACT

Blocking mitotic progression has been proposed as an attractive therapeutic strategy to impair proliferation of tumour cells. However, how cells survive during prolonged mitotic arrest is not well understood. We show here that survival during mitotic arrest is affected by the special energetic requirements of mitotic cells. Prolonged mitotic arrest results in mitophagy-dependent loss of mitochondria, accompanied by reduced ATP levels and the activation of AMPK. Oxidative respiration is replaced by glycolysis owing to AMPK-dependent phosphorylation of PFKFB3 and increased production of this protein as a consequence of mitotic-specific translational activation of its mRNA. Induction of autophagy or inhibition of AMPK or PFKFB3 results in enhanced cell death in mitosis and improves the anti-tumoral efficiency of microtubule poisons in breast cancer cells. Thus, survival of mitotic-arrested cells is limited by their metabolic requirements, a feature with potential implications in cancer therapies aimed to impair mitosis or metabolism in tumour cells. More... »

PAGES

1304-1316

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/ncb3231

    DOI

    http://dx.doi.org/10.1038/ncb3231

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1001470569

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/26322680


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