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Cancers
Special Issues
Targeting Mitochondria in Anti-tumor Drug Development
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Targeting Mitochondria in Anti-tumor Drug Development

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

Deadline for manuscript submissions: 15 June 2024 | Viewed by 2065

Special Issue Editors

Dr. Bela Ozsvari

E-Mail Website
Guest Editor
Translational Medicine, School of Science, Engineering and Environment (SEE), University of Salford, Manchester, UK
Interests: breast cancer; mitochondria; cancer stem cells; senescence; drug screening
Special Issues, Collections and Topics in MDPI journals
Dr. Nadia J. Jacobo-Herrera

E-Mail Website
Guest Editor
Biochemistry Unit, National Nutrition Institute of Mexico (Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán), Mexico City, Mexico
Interests: colon cancer; cancer metabolism; natural products; drug repositioning
Special Issues, Collections and Topics in MDPI journals
Dr. Carlos Pérez-Plasencia

E-Mail Website
Guest Editor
1. Laboratorio de Genómica, Instituto Nacional de Cancerología, Tlalpan, Mexico
2. Laboratorio de Genómica Funcional, Unidad de Biomedicina, FES-IZTACALA, Universidad Nacional Autónoma de México, Tlalnepantla, Mexico
Interests: cancer genomics studies; transcriptional programs; genetic-chromosomal aberrations; metabolism and mitochondrial genes; autophagy and mitophagy as therapeutic strategies in cancer

Special Issue Information

Dear Colleagues,

Metabolic reprogramming in cancer is a well-known phenomenon and experimental evidence demonstrates that invasive migratory cancer cells often switch to elevated mitochondrial metabolism, which is not the primary target of current oncotherapies, often resulting in a poor outcome or relapse. Thus, the development of novel anti-cancer drugs or repurposing of known medicines targeting tumor metabolism can be promising anticancer strategies.

The purpose of this Special Issue is to discuss the latest research into drug development targeting tumor metabolism, particularly focusing on metabolic vulnerabilities in mitochondria. Original research articles as well as reviews are welcome.

Dr. Bela Ozsvari
Dr. Nadia J. Jacobo-Herrera
Dr. Carlos Pérez-Plasencia
Guest Editors

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

  • cancer metabolism
  • mitochondria
  • metabolic reprogramming
  • anti-tumor drug development

Published Papers (2 papers)

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Research

21 pages, 5459 KiB  
Article
Inhibition of Carbohydrate Metabolism Potentiated by the Therapeutic Effects of Oxidative Phosphorylation Inhibitors in Colon Cancer Cells
by Lichao Guo, Baochen Zhang, Wen Zhang, Yanqi Xie, Xi Chen, Xueke Sun, David S. Watt, Chunming Liu, H. Peter Spielmann and Xifu Liu
Cancers 2024, 16(7), 1399; https://doi.org/10.3390/cancers16071399 - 02 Apr 2024
Viewed by 905
Abstract
Cancer cells undergo a significant level of “metabolic reprogramming” or “remodeling” to ensure an adequate supply of ATP and “building blocks” for cell survival and to facilitate accelerated proliferation. Cancer cells preferentially use glycolysis for ATP production (the Warburg effect); however, cancer cells, [...] Read more.
Cancer cells undergo a significant level of “metabolic reprogramming” or “remodeling” to ensure an adequate supply of ATP and “building blocks” for cell survival and to facilitate accelerated proliferation. Cancer cells preferentially use glycolysis for ATP production (the Warburg effect); however, cancer cells, including colorectal cancer (CRC) cells, also depend on oxidative phosphorylation (OXPHOS) for ATP production, a finding that suggests that both glycolysis and OXPHOS play significant roles in facilitating cancer progression and proliferation. Our prior studies identified a semisynthetic isoflavonoid, DBI-1, that served as an AMPK activator targeting mitochondrial complex I. Furthermore, DBI-1 and a glucose transporter 1 (GLUT1) inhibitor, BAY-876, synergistically inhibited CRC cell growth in vitro and in vivo. We now report a study of the structure–activity relationships (SARs) in the isoflavonoid family in which we identified a new DBI-1 analog, namely, DBI-2, with promising properties. Here, we aimed to explore the antitumor mechanisms of DBIs and to develop new combination strategies by targeting both glycolysis and OXPHOS. We identified DBI-2 as a novel AMPK activator using an AMPK phosphorylation assay as a readout. DBI-2 inhibited mitochondrial complex I in the Seahorse assays. We performed proliferation and Western blotting assays and conducted studies of apoptosis, necrosis, and autophagy to corroborate the synergistic effects of DBI-2 and BAY-876 on CRC cells in vitro. We hypothesized that restricting the carbohydrate uptake with a KD would mimic the effects of GLUT1 inhibitors, and we found that a ketogenic diet significantly enhanced the therapeutic efficacy of DBI-2 in CRC xenograft mouse models, an outcome that suggested a potentially new approach for combination cancer therapy. Full article
(This article belongs to the Special Issue Targeting Mitochondria in Anti-tumor Drug Development)
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17 pages, 15254 KiB  
Article
Laherradurin Inhibits Tumor Growth in an Azoxymethane/Dextran Sulfate Sodium Colorectal Cancer Model In Vivo
by Michael Joshue Rendón-Barrón, Eduardo Pérez-Arteaga, Izamary Delgado-Waldo, Jossimar Coronel-Hernández, Carlos Pérez-Plasencia, Frida Rodríguez-Izquierdo, Rosa Linares, Alma Rosa González-Esquinca, Isela Álvarez-González, Eduardo Madrigal-Bujaidar and Nadia Judith Jacobo-Herrera
Cancers 2024, 16(3), 573; https://doi.org/10.3390/cancers16030573 - 29 Jan 2024
Viewed by 882
Abstract
Colorectal cancer (CRC) is the third most common neoplasia in the world. Its mortality rate is high due to the lack of specific and effective treatments, metastasis, and resistance to chemotherapy, among other factors. The natural products in cancer are a primary source [...] Read more.
Colorectal cancer (CRC) is the third most common neoplasia in the world. Its mortality rate is high due to the lack of specific and effective treatments, metastasis, and resistance to chemotherapy, among other factors. The natural products in cancer are a primary source of bioactive molecules. In this research, we evaluated the antitumor activity of an acetogenin (ACG), laherradurin (LH), isolated from the Mexican medicinal plant Annona macroprophyllata Donn.Sm. in a CRC murine model. The CRC was induced by azoxymethane–dextran sulfate sodium (AOM/DSS) in Balb/c mice and treated for 21 days with LH or cisplatin. This study shows for the first time the antitumor activity of LH in an AOM/DSS CRC model. The acetogenin diminished the number and size of tumors compared with cisplatin; the histologic studies revealed a recovery of the colon tissue, and the blood toxicity data pointed to less damage in animals treated with LH. The TUNEL assay indicated cell death by apoptosis, and the in vitro studies exhibited that LH inhibited cell migration in HCT116 cells. Our study provides strong evidence of a possible anticancer agent for CRC. Full article
(This article belongs to the Special Issue Targeting Mitochondria in Anti-tumor Drug Development)
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