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Drug Metabolism in Cancer Therapy
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Drug Metabolism in Cancer Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 12812

Special Issue Editors

Dr. Nuno Vale

E-Mail Website
Guest Editor
Department of Community Medicine, Health Information and Decision, Faculty of Medicine, University of Porto, Rua Dr. Plácido da Costa, 4200-450 Porto, Portugal
Interests: in silico pharmacology; PBPK; drug metabolism; drug combination; drug delivery; peptides; ADME; DMPK; pharmacokinetic
Special Issues, Collections and Topics in MDPI journals
Dr. Swaroop Kumar Pandey

E-Mail Website
Guest Editor
National Institute for Biotechnology in the Negev, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel
Interests: drug discovery; molecular oncology; biomarker

Special Issue Information

Dear Colleagues,

There seems to be a consensus that alterations in cellular metabolism are a hallmark of cancer cells, and rewired metabolism is essential for rapid tumor growth and proliferation. Cancer cells sustain their high glycolytic rates in several ways and it is becoming increasingly clear that changes in metabolism influence drug response to established first-line chemotherapy in several cancers, identifying metabolic rewiring as a novel, and important mechanism of adaptive resistance. Furthermore, drug-metabolizing enzymes in tumors are capable of biotransforming a variety of xenobiotics, including drugs, resulting in either their activation or detoxification.Knowing the metabolism of drugs in a normal or tumor cell environment can influence the intervention capacity of their use, per se or in combination. Understanding how the resistance of drugs can be prevented can be important to improving cancer therapy.

We look forward to receiving research articles and comprehensive reviews related (but not limited) to the following topics:

  • Cancer Therapy
  • Drug Metabolism
  • Cellular Metabolism
  • Metabolism and Drug Resistance
  • Energy Metabolism
  • Drug-Drug Interaction

Prof. Dr. Nuno Vale
Dr. Swaroop Kumar Pandey
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • drug resistance
  • cancer therapy
  • biomarkers for drug resitance
  • molecular mechanisms
  • drug-drug interaction

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Published Papers (3 papers)

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Research

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14 pages, 2896 KiB  
Article
Counteracting Colon Cancer by Inhibiting Mitochondrial Respiration and Glycolysis with a Selective PKCδ Activator
by Cláudia Bessa, Joana B. Loureiro, Matilde Barros, Vera M. S. Isca, Vilma A. Sardão, Paulo J. Oliveira, Raquel L. Bernardino, Carina Herman-de-Sousa, Maria Adelina Costa, Paulo Correia-de-Sá, Marco G. Alves, Patrícia Rijo and Lucília Saraiva
Int. J. Mol. Sci. 2023, 24(6), 5710; https://doi.org/10.3390/ijms24065710 - 16 Mar 2023
Cited by 1 | Viewed by 3000
Abstract
Metabolic reprogramming is a central hub in tumor development and progression. Therefore, several efforts have been developed to find improved therapeutic approaches targeting cancer cell metabolism. Recently, we identified the 7α-acetoxy-6β-benzoyloxy-12-O-benzoylroyleanone (Roy-Bz) as a PKCδ-selective activator with [...] Read more.
Metabolic reprogramming is a central hub in tumor development and progression. Therefore, several efforts have been developed to find improved therapeutic approaches targeting cancer cell metabolism. Recently, we identified the 7α-acetoxy-6β-benzoyloxy-12-O-benzoylroyleanone (Roy-Bz) as a PKCδ-selective activator with potent anti-proliferative activity in colon cancer by stimulating a PKCδ-dependent mitochondrial apoptotic pathway. Herein, we investigated whether the antitumor activity of Roy-Bz, in colon cancer, could be related to glucose metabolism interference. The results showed that Roy-Bz decreased the mitochondrial respiration in human colon HCT116 cancer cells, by reducing electron transfer chain complexes I/III. Consistently, this effect was associated with downregulation of the mitochondrial markers cytochrome c oxidase subunit 4 (COX4), voltage-dependent anion channel (VDAC) and mitochondrial import receptor subunit TOM20 homolog (TOM20), and upregulation of synthesis of cytochrome c oxidase 2 (SCO2). Roy-Bz also dropped glycolysis, decreasing the expression of critical glycolytic markers directly implicated in glucose metabolism such as glucose transporter 1 (GLUT1), hexokinase 2 (HK2) and monocarboxylate transporter 4 (MCT4), and increasing TP53-induced glycolysis and apoptosis regulator (TIGAR) protein levels. These results were further corroborated in tumor xenografts of colon cancer. Altogether, using a PKCδ-selective activator, this work evidenced a potential dual role of PKCδ in tumor cell metabolism, resulting from the inhibition of both mitochondrial respiration and glycolysis. Additionally, it reinforces the antitumor therapeutic potential of Roy-Bz in colon cancer by targeting glucose metabolism. Full article
(This article belongs to the Special Issue Drug Metabolism in Cancer Therapy)
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Review

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13 pages, 576 KiB  
Review
Dual Drug Repurposing: The Example of Saracatinib
by Raquel Ramos and Nuno Vale
Int. J. Mol. Sci. 2024, 25(8), 4565; https://doi.org/10.3390/ijms25084565 - 22 Apr 2024
Cited by 1 | Viewed by 2055
Abstract
Saracatinib (AZD0530) is a dual Src/Abl inhibitor initially developed by AstraZeneca for cancer treatment; however, data from 2006 to 2024 reveal that this drug has been tested not only for cancer treatment, but also for the treatment of other diseases. Despite the promising [...] Read more.
Saracatinib (AZD0530) is a dual Src/Abl inhibitor initially developed by AstraZeneca for cancer treatment; however, data from 2006 to 2024 reveal that this drug has been tested not only for cancer treatment, but also for the treatment of other diseases. Despite the promising pre-clinical results and the tolerability shown in phase I trials, where a maximum tolerated dose of 175 mg was defined, phase II clinical data demonstrated a low therapeutic action against several cancers and an elevated rate of adverse effects. Recently, pre-clinical research aimed at reducing the toxic effects and enhancing the therapeutic performance of saracatinib using nanoparticles and different pharmacological combinations has shown promising results. Concomitantly, saracatinib was repurposed to treat Alzheimer’s disease, targeting Fyn. It showed great clinical results and required a lower daily dose than that defined for cancer treatment, 125 mg and 175 mg, respectively. In addition to Alzheimer’s disease, this Src inhibitor has also been studied in relation to other health conditions such as pulmonary and liver fibrosis and even for analgesic and anti-allergic functions. Although saracatinib is still not approved by the Food and Drug Administration (FDA), the large number of alternative uses for saracatinib and the elevated number of pre-clinical and clinical trials performed suggest the huge potential of this drug for the treatment of different kinds of diseases. Full article
(This article belongs to the Special Issue Drug Metabolism in Cancer Therapy)
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21 pages, 997 KiB  
Review
Mechanisms of Resistance to Antibody-Drug Conjugates
by Rita Khoury, Khalil Saleh, Nadine Khalife, Mohamad Saleh, Claude Chahine, Rebecca Ibrahim and Axel Lecesne
Int. J. Mol. Sci. 2023, 24(11), 9674; https://doi.org/10.3390/ijms24119674 - 2 Jun 2023
Cited by 28 | Viewed by 6743
Abstract
The treatment of cancer patients has dramatically changed over the past decades with the advent of monoclonal antibodies, immune-checkpoint inhibitors, bispecific antibodies, and innovative T-cell therapy. Antibody-drug conjugates (ADCs) have also revolutionized the treatment of cancer. Several ADCs have already been approved in [...] Read more.
The treatment of cancer patients has dramatically changed over the past decades with the advent of monoclonal antibodies, immune-checkpoint inhibitors, bispecific antibodies, and innovative T-cell therapy. Antibody-drug conjugates (ADCs) have also revolutionized the treatment of cancer. Several ADCs have already been approved in hematology and clinical oncology, such as trastuzumab emtansine (T-DM1), trastuzumab deruxtecan (T-DXd), and sacituzumab govitecan (SG) for the treatment of metastatic breast cancer, and enfortumab vedotin (EV) for the treatment of urothelial carcinoma. The efficacy of ADCs is limited by the emergence of resistance due to different mechanisms, such as antigen-related resistance, failure of internalization, impaired lysosomal function, and other mechanisms. In this review, we summarize the clinical data that contributed to the approval of T-DM1, T-DXd, SG, and EV. We also discuss the different mechanisms of resistance to ADCs, as well as the ways to overcome this resistance, such as bispecific ADCs and the combination of ADCs with immune-checkpoint inhibitors or tyrosine-kinase inhibitors. Full article
(This article belongs to the Special Issue Drug Metabolism in Cancer Therapy)
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