Mitochondrial Metabolism and Cancer

Dear Colleagues,

Mitochondria are central regulators of cellular energy metabolism, biosynthesis, and signaling. Far beyond their classical role as “powerhouses of the cell,” mitochondria integrate metabolic networks that sustain proliferation, control cell death, and influence the tumor microenvironment. In cancer, mitochondrial metabolism undergoes profound remodeling, enabling tumor cells to adapt to fluctuating nutrient availability, resist therapeutic stress, and promote invasion and metastasis. These metabolic adaptations are increasingly recognized not as passive consequences of malignant transformation but as active drivers of tumorigenesis and disease progression. Understanding how mitochondria contribute to cancer biology is therefore critical for uncovering novel biomarkers, therapeutic vulnerabilities, and strategies for personalized medicine.

This Special Issue, “Mitochondrial Metabolism and Cancer”, aims to bring together cutting-edge contributions that advance our knowledge of the diverse and dynamic roles of mitochondria in cancer. We welcome both original research articles and comprehensive reviews addressing mitochondrial function across different tumor types and cellular contexts. Of particular interest are studies employing systems-level approaches, such as mitochondrial proteomics, metabolomics, genomics, and lipidomics, to dissect the complexity of mitochondrial pathways and their regulation in cancer cells.

We also encourage submissions exploring how experimental treatments, including natural and synthetic molecules, modulate mitochondrial metabolism in cancer models. Work that connects mitochondrial rewiring with therapeutic response or resistance, tumor heterogeneity, and immune evasion is highly relevant. Similarly, studies that identify novel mitochondrial targets, characterize mitochondrial dynamics (fusion, fission, mitophagy), or investigate the role of mitochondria in metabolic cross-talk with the tumor microenvironment are welcome.

By bringing together these diverse perspectives, this Special Issue seeks to highlight the central role of mitochondria in shaping cancer phenotypes and to provide an integrative platform for discussing therapeutic opportunities arising from mitochondrial biology. We invite contributions that will deepen our understanding of how mitochondrial metabolism influences tumor development and treatment, with the ultimate goal of translating this knowledge into innovative strategies to combat cancer.

Both original research and reviews are welcome in this Special Issue.

Prof. Dr. Marcos Roberto de Oliveira
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.