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Herrera et al. J Cancer Metastasis Treat 2018;4:42 Journal of Cancer
DOI: 10.20517/2394-4722.2018.35 Metastasis and Treatment

Review Open Access

Genomic heterogeneity meets cellular energetics:
crosstalk between the mitochondria and the cell

cycle

Erica L. Herrera, Seham Z. Azzam, Madison C. Berger, Laura A. Diaz-Martinez

Department of Biological Sciences, The University of Texas at El Paso, El Paso, TX 79968, USA.
Correspondence to: Dr. Laura A. Diaz-Martinez, Department of Biological Sciences, The University of Texas at El Paso, 500
West University Avenue, El Paso, TX 79968, USA. E-mail: ladiazmartinez@utep.edu
How to cite this article: Herrera EL, Azzam SZ, Berger MC, Diaz-Martinez LA. Genomic heterogeneity meets cellular energetics:
crosstalk between the mitochondria and the cell cycle. J Cancer Metastasis Treat 2018;4:42.
http://dx.doi.org/10.20517/2394-4722.2018.35

Received: 3 Jun 2018 First Decision: 5 Jul 2018 Revised: 12 Jul 2018 Accepted: 19 Jul 2018 Published: 6 Aug 2018
Science Editor: Yi-Hong Zhou Copy Editor: Jun-Yao Li Production Editor: Cai-Hong Wang

Abstract
Changes in cellular energetics and genomic instability are two characteristics of cancers that have been studied
independently. Evidence of cross-talk between mitochondria function and nuclear function has started to emerge,
suggesting that these pathways can influence one another. Here we review recent evidence that links the mitochondria
and the cell cycle. This evidence indicates bidirectional cross-talk where mitochondria function can regulate the
cell cycle and induce genomic instability, and conversely, the cell cycle machinery regulates mitochondria function.
Implications for this cross-talk in the development of cancer are discussed.

Keywords: Mitochondria dynamics, cell cycle, mitochondria heterogeneity, genomic heterogeneity

INTRODUCTION
Changes in metabolism and genomic instability were among the earliest characteristics of tumors to be
identified. Boveri’s hypothesis in the early 1900s that malignant tumors originated from cells with abnormal
chromosome numbers , initiated an era of research on the role of genomic instability in cancer development.
[1]
Likewise, Otto Warburg’s work on the metabolic changes in tumor cells pioneered an era of research
[2,3]
studying the role of changes in cell metabolism during cancer progression. These two fields, however, have
mostly remained separate. Here we focus on emerging evidence of crosstalk between the processes occurring
at the mitochondria and those in the nucleus, particularly as it relates to the cell cycle. These discoveries

© The Author(s) 2018. Open Access This article is licensed under a Creative Commons Attribution 4.0
International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
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and indicate if changes were made.

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