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Cancers
Special Issues
Mitochondria as Targets for Cancer Therapy
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Mitochondria as Targets for Cancer Therapy

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 3251

Special Issue Editor

Prof. Dr. Donat Kögel

E-Mail Website
Guest Editor
Experimental Neurosurgery, Neuroscience Center, Goethe-University Frankfurt, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany
Interests: brain tumors; intrinsic and acquired therapy resistance; apoptosis; autophagy; mitochondria as targets for cancer therapy; mechanisms of tumor cell migration and invasion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Mitochondria, organelles that serve as the power houses of the cell, are the primary source of cellular ATP generated via the OXPHOS pathway that is linked to the tricarboxylic acid cycle (TCA) and fatty acid oxidation. In addition to their key function in maintaining cellular metabolism and bioenergetics, mitochondria have important roles in the regulation of apoptosis, innate immunity, as well as calcium and redox homeostasis. Mitochondria are main sources of reactive oxygen species (ROS), and mitochondrial dysfunction is linked to cellular aging and different pathologies, including myopathies, neurodegeneration, and tumorigenesis/cancer. Given their multifunctional roles, mitochondria have long been considered highly relevant targets for cancer therapy, with mitochondria-targeting agents (termed mitocans) directed against different mitochondrial components/functions, including respiratory chain complexes (OXPHOS inhibitors), apoptosis (BH3 mimetics), oncometabolites (IDH-mutant inhibitors), as well as mitophagy, the selective removal of damaged mitochondria via the autophagy pathway. Several mitocans have already entered the clinical stage, the biggest success story so far being the Bcl-2 inhibitor Venetoclax (ABT-199) that is approved for the treatment of chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), and acute myeloic leukemia (AML). New and ongoing experimental studies will hopefully lead to the identification of additional and highly effective novel drugs/approaches to target mitochondria in different cancer entities, including solid tumors in the foreseeable future. We would like to invite both original research and review articles highlighting recent advances in this exciting field of research.

Prof. Dr. Donat Kögel
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 short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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.

Keywords

  • mitochondria oxidative phosphorlyation
  • glycolysis
  • tumor cell metabolism
  • metabolic adaptation
  • redox homeostasis
  • apoptosis
  • autophagy
  • innate immunity

Published Papers (2 papers)

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Research

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13 pages, 1420 KiB  
Article
Knockdown of Antisense Noncoding Mitochondrial RNA Reduces Tumorigenicity of Patient-Derived Clear Cell Renal Carcinoma Cells in an Orthotopic Xenograft Mouse Model
by Mariela Araya, Francisca Sepúlveda, Jaime Villegas, Luis Alarcón, Luis O. Burzio, Verónica A. Burzio and Vincenzo Borgna
Cancers 2024, 16(4), 830; https://doi.org/10.3390/cancers16040830 - 19 Feb 2024
Viewed by 1007
Abstract
Clear cell renal cell carcinoma (ccRCC) is the most prevalent form of renal cancer and its treatment is hindered by a resistance to targeted therapies, immunotherapies and combinations of both. We have reported that the knockdown of the antisense noncoding mitochondrial RNAs (ASncmtRNAs) [...] Read more.
Clear cell renal cell carcinoma (ccRCC) is the most prevalent form of renal cancer and its treatment is hindered by a resistance to targeted therapies, immunotherapies and combinations of both. We have reported that the knockdown of the antisense noncoding mitochondrial RNAs (ASncmtRNAs) with chemically modified antisense oligonucleotides induces proliferative arrest and apoptotic death in tumor cells from many human and mouse cancer types. These studies have been mostly performed in vitro and in vivo on commercially available cancer cell lines and have shown that in mouse models tumor growth is stunted by the treatment. The present work was performed on cells derived from primary and metastatic ccRCC tumors. We established primary cultures from primary and metastatic ccRCC tumors, which were subjected to knockdown of ASncmtRNAs in vitro and in vivo in an orthotopic xenograft model in NOD/SCID mice. We found that these primary ccRCC cells are affected in the same way as tumor cell lines and in the orthotopic model tumor growth was significantly reduced by the treatment. This study on patient-derived ccRCC tumor cells represents a model closer to actual patient ccRCC tumors and shows that knockdown of ASncmtRNAs poses a potential treatment option for these patients. Full article
(This article belongs to the Special Issue Mitochondria as Targets for Cancer Therapy)
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Review

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20 pages, 1748 KiB  
Review
Mitochondrial Metabolism: A New Dimension of Personalized Oncology
by Babak Behnam and Farzad Taghizadeh-Hesary
Cancers 2023, 15(16), 4058; https://doi.org/10.3390/cancers15164058 - 11 Aug 2023
Cited by 9 | Viewed by 1620
Abstract
Energy is needed by cancer cells to stay alive and communicate with their surroundings. The primary organelles for cellular metabolism and energy synthesis are mitochondria. Researchers recently proved that cancer cells can steal immune cells’ mitochondria using nanoscale tubes. This finding demonstrates the [...] Read more.
Energy is needed by cancer cells to stay alive and communicate with their surroundings. The primary organelles for cellular metabolism and energy synthesis are mitochondria. Researchers recently proved that cancer cells can steal immune cells’ mitochondria using nanoscale tubes. This finding demonstrates the dependence of cancer cells on normal cells for their living and function. It also denotes the importance of mitochondria in cancer cells’ biology. Emerging evidence has demonstrated how mitochondria are essential for cancer cells to survive in the harsh tumor microenvironments, evade the immune system, obtain more aggressive features, and resist treatments. For instance, functional mitochondria can improve cancer resistance against radiotherapy by scavenging the released reactive oxygen species. Therefore, targeting mitochondria can potentially enhance oncological outcomes, according to this notion. The tumors’ responses to anticancer treatments vary, ranging from a complete response to even cancer progression during treatment. Therefore, personalized cancer treatment is of crucial importance. So far, personalized cancer treatment has been based on genomic analysis. Evidence shows that tumors with high mitochondrial content are more resistant to treatment. This paper illustrates how mitochondrial metabolism can participate in cancer resistance to chemotherapy, immunotherapy, and radiotherapy. Pretreatment evaluation of mitochondrial metabolism can provide additional information to genomic analysis and can help to improve personalized oncological treatments. This article outlines the importance of mitochondrial metabolism in cancer biology and personalized treatments. Full article
(This article belongs to the Special Issue Mitochondria as Targets for Cancer Therapy)
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