Cyclin B1/CDK1-regulated mitochondrial bioenergetics in cell cycle progression and tumor resistance

Bowen Xie, Shuangyan Wang, Nian Jiang, Jian-Jian Li

Research output: Contribution to journalShort survey

Abstract

A mammalian cell houses two genomes located separately in the nucleus and mitochondria. During evolution, communications and adaptations between these two genomes occur extensively to achieve and sustain homeostasis for cellular functions and regeneration. Mitochondria provide the major cellular energy and contribute to gene regulation in the nucleus, whereas more than 98% of mitochondrial proteins are encoded by the nuclear genome. Such two-way signaling traffic presents an orchestrated dynamic between energy metabolism and consumption in cells. Recent reports have elucidated the way how mitochondrial bioenergetics synchronizes with the energy consumption for cell cycle progression mediated by cyclin B1/CDK1 as the communicator. This review is to recapitulate cyclin B1/CDK1 mediated mitochondrial activities in cell cycle progression and stress response as well as its potential link to reprogram energy metabolism in tumor adaptive resistance. Cyclin B1/CDK1-mediated mitochondrial bioenergetics is applied as an example to show how mitochondria could timely sense the cellular fuel demand and then coordinate ATP output. Such nucleus-mitochondria oscillation may play key roles in the flexible bioenergetics required for tumor cell survival and compromising the efficacy of anti-cancer therapy. Further deciphering the cyclin B1/CDK1-controlled mitochondrial metabolism may invent effect targets to treat resistant cancers.

LanguageEnglish (US)
Pages56-66
Number of pages11
JournalCancer Letters
Volume443
DOIs
StatePublished - Feb 28 2019

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Cyclin B1
Energy Metabolism
Cell Cycle
Mitochondria
Genome
Neoplasms
Mitochondrial Proteins
Regeneration
Cell Survival
Homeostasis
Adenosine Triphosphate
Genes

Keywords

  • CDK
  • Cell cycle
  • Metabolism
  • Mitochondria
  • Tumor resistance

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Cyclin B1/CDK1-regulated mitochondrial bioenergetics in cell cycle progression and tumor resistance. / Xie, Bowen; Wang, Shuangyan; Jiang, Nian; Li, Jian-Jian.

In: Cancer Letters, Vol. 443, 28.02.2019, p. 56-66.

Research output: Contribution to journalShort survey

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AU - Li, Jian-Jian

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AB - A mammalian cell houses two genomes located separately in the nucleus and mitochondria. During evolution, communications and adaptations between these two genomes occur extensively to achieve and sustain homeostasis for cellular functions and regeneration. Mitochondria provide the major cellular energy and contribute to gene regulation in the nucleus, whereas more than 98% of mitochondrial proteins are encoded by the nuclear genome. Such two-way signaling traffic presents an orchestrated dynamic between energy metabolism and consumption in cells. Recent reports have elucidated the way how mitochondrial bioenergetics synchronizes with the energy consumption for cell cycle progression mediated by cyclin B1/CDK1 as the communicator. This review is to recapitulate cyclin B1/CDK1 mediated mitochondrial activities in cell cycle progression and stress response as well as its potential link to reprogram energy metabolism in tumor adaptive resistance. Cyclin B1/CDK1-mediated mitochondrial bioenergetics is applied as an example to show how mitochondria could timely sense the cellular fuel demand and then coordinate ATP output. Such nucleus-mitochondria oscillation may play key roles in the flexible bioenergetics required for tumor cell survival and compromising the efficacy of anti-cancer therapy. Further deciphering the cyclin B1/CDK1-controlled mitochondrial metabolism may invent effect targets to treat resistant cancers.

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