Asset Details
Do you wish to reserve the book?
AMPK and PFKFB3 mediate glycolysis and survival in response to mitophagy during mitotic arrest
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
AMPK and PFKFB3 mediate glycolysis and survival in response to mitophagy during mitotic arrest
Do you wish to request the book?
AMPK and PFKFB3 mediate glycolysis and survival in response to mitophagy during mitotic arrest
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
AMPK and PFKFB3 mediate glycolysis and survival in response to mitophagy during mitotic arrest
2015
Overview
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.
Malumbres and colleagues reveal that mitotic arrest is accompanied by reduced mitochondrial mass and oxidative respiration resulting in activation of AMPK and induction of glycolysis to promote cell survival.
Publisher
Nature Publishing Group UK,Nature Publishing Group
Subject
/ 13/89
/ 14/28
/ 14/33
/ 38/77
/ 42/35
/ 64/60
/ 82/80
/ 96/106
/ 96/109
/ 96/31
/ 96/34
/ 96/63
/ 96/95
/ AMP-Activated Protein Kinases - genetics
/ AMP-Activated Protein Kinases - metabolism
/ Animals
/ Antineoplastic Agents - pharmacology
/ Cancer
/ Cell Survival - drug effects
/ Embryo, Mammalian - cytology
/ Embryo, Mammalian - metabolism
/ Enzymes
/ Female
/ Fibroblasts - ultrastructure
/ Humans
/ M Phase Cell Cycle Checkpoints - genetics
/ M Phase Cell Cycle Checkpoints - physiology
/ Methods
/ Mitosis
/ Phosphofructokinase-2 - genetics
/ Phosphofructokinase-2 - metabolism
/ Poisons
