PUBLICATIONS

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Authors:

Giulia Leone, Houda Abla, Giuseppe Gasparre, Anna Maria Porcelli and Luisa Iommarini

Journal: 

Genes 2018, 9(5), 243; https://doi.org/10.3390/genes9050243

Received: 9 April 2018; Accepted: 3 May 2018; Published: 7 May 2018.

Abstract: Mitochondrial respiratory function is now recognized as a pivotal player in all the aspects of cancer biology, from tumorigenesis to aggressiveness and chemotherapy resistance. Among the enzymes that compose the respiratory chain, by contributing to energy production, redox equilibrium and oxidative stress, complex I assumes a central role. Complex I defects may arise from mutations in mitochondrial or nuclear DNA, in both structural genes or assembly factors, from alteration of the expression levels of its subunits, or from drug exposure. Since cancer cells have a high-energy demand and require macromolecules for proliferation, it is not surprising that severe complex I defects, caused either by mutations or treatment with specific inhibitors, prevent tumor progression, while contributing to resistance to certain chemotherapeutic agents. On the other hand, enhanced oxidative stress due to mild complex I dysfunction drives an opposite phenotype, as it stimulates cancer cell proliferation and invasiveness. We here review the current knowledge on the contribution of respiratory complex I to cancer biology, highlighting the double-edged role of this metabolic enzyme in tumor progression, metastasis formation, and response to chemotherapy.

Keywords: respiratory complex I; mtDNA; mitochondria; mtDNA mutations; cancer; tumor progression; oncojanus

Full text available at: http://www.mdpi.com/2073-4425/9/5/243/htm