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Cancers
Special Issues
Cancer Cell Metabolism and Drug Targets
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Cancer Cell Metabolism and Drug Targets

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

Deadline for manuscript submissions: 30 June 2024 | Viewed by 3854

Special Issue Editors

Dr. Daniel S. Sitar

E-Mail Website
Guest Editor
Department of Pharmacology and Therapeutics, University of Manitoba, A205B-753 McDermot Ave., Winnipeg, MB R3E 0T6, Canada
Interests: drug metabolism; cancer diagnoses; metabolomics
Prof. Dr. Donald Miller

E-Mail Website
Guest Editor
Department of Pharmacology & Therapeutics, University of Manitoba, A205-753 McDermot Ave. Winnipeg, MB R3E 0T6, Canada
Interests: brain tumors; blood/brain barrier; biomarkers

Special Issue Information

Dear Colleagues,

Cancer incidence and prevalence continue to increase. The recent focus on cancer cell metabolism and metabolomics has demonstrated that tissue tumor-driven changes in the profile of circulating small molecules in biological fluids can occur. These alterations in the metabolic profile offer potential for the early detection of cancer, identification of selective drug targets that may attack specific vulnerabilities, as well as a means for real-time monitoring of tumor response to therapy. These patterns appear to offer potential for the identification of selective drug targets that may attack tumor vulnerabilities.

The purpose of this Special Issue is to invite reviews and/or original research findings on cancer cell metabolic pathways that characterize further cancer cell metabolic pathways that can be used for tracking tumor progression and guiding current and future therapeutic interventions.

Dr. Daniel S. Sitar
Prof. Dr. Donald Miller
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

  • metabolomics
  • cancer staging
  • tumor sensitization
  • biomarkers
  • tumor cell metabolism

Published Papers (3 papers)

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Research

29 pages, 7537 KiB  
Article
Mutation Status and Glucose Availability Affect the Response to Mitochondria-Targeted Quercetin Derivative in Breast Cancer Cells
by Paweł Przybylski, Anna Lewińska, Iwona Rzeszutek, Dominika Błoniarz, Aleksandra Moskal, Gabriela Betlej, Anna Deręgowska, Martyna Cybularczyk-Cecotka, Tomasz Szmatoła, Grzegorz Litwinienko and Maciej Wnuk
Cancers 2023, 15(23), 5614; https://doi.org/10.3390/cancers15235614 - 28 Nov 2023
Cited by 1 | Viewed by 1162
Abstract
Mitochondria, the main cellular power stations, are important modulators of redox-sensitive signaling pathways that may determine cell survival and cell death decisions. As mitochondrial function is essential for tumorigenesis and cancer progression, mitochondrial targeting has been proposed as an attractive anticancer strategy. In [...] Read more.
Mitochondria, the main cellular power stations, are important modulators of redox-sensitive signaling pathways that may determine cell survival and cell death decisions. As mitochondrial function is essential for tumorigenesis and cancer progression, mitochondrial targeting has been proposed as an attractive anticancer strategy. In the present study, three mitochondria-targeted quercetin derivatives (mitQ3, 5, and 7) were synthesized and tested against six breast cancer cell lines with different mutation and receptor status, namely ER-positive MCF-7, HER2-positive SK-BR-3, and four triple-negative (TNBC) cells, i.e., MDA-MB-231, MDA-MB-468, BT-20, and Hs 578T cells. In general, the mito-quercetin response was modulated by the mutation status. In contrast to unmodified quercetin, 1 µM mitQ7 induced apoptosis in breast cancer cells. In MCF-7 cells, mitQ7-mediated apoptosis was potentiated under glucose-depleted conditions and was accompanied by elevated mitochondrial superoxide production, while AMPK activation-based energetic stress was associated with the alkalization of intracellular milieu and increased levels of NSUN4. Mito-quercetin also eliminated doxorubicin-induced senescent breast cancer cells, which was accompanied by the depolarization of mitochondrial transmembrane potential. Limited glucose availability also sensitized doxorubicin-induced senescent breast cancer cells to apoptosis. In conclusion, we show an increased cytotoxicity of mitochondria-targeted quercetin derivatives compared to unmodified quercetin against breast cancer cells with different mutation status that can be potentiated by modulating glucose availability. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism and Drug Targets)
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19 pages, 4159 KiB  
Article
Targeting Esophageal Squamous Cell Carcinoma by Combining Copper Ionophore Disulfiram and JMJD3/UTX Inhibitor GSK J4
by Canlin Yang, Fei Li, Yuanyuan Ren, Qianqian Zhang, Bo Jiao, Jianming Zhang and Junxing Huang
Cancers 2023, 15(22), 5347; https://doi.org/10.3390/cancers15225347 - 9 Nov 2023
Viewed by 914
Abstract
The alcohol-averse drug disulfiram has been reported to have anti-tumor effects and is well suited for drug combinations. In order to identify potential drug combinations in esophageal squamous cell carcinoma (ESCC), we screened a bioactive compound library with the disulfiram copper chelation product [...] Read more.
The alcohol-averse drug disulfiram has been reported to have anti-tumor effects and is well suited for drug combinations. In order to identify potential drug combinations in esophageal squamous cell carcinoma (ESCC), we screened a bioactive compound library with the disulfiram copper chelation product CuET. The Jumonji domain-containing protein 3 (JMJD3) and the ubiquitously transcribed tetratricopeptide repeat protein X-linked (UTX) inhibitor GSK J4 were identified. To further understand the molecular mechanism underlying the efficient drug combination, we applied quantitative mass spectrometry to analyze the signaling pathway perturbation after drug treatment. The data revealed that the synergistic effect of GSK J4 and CuET was due to the interaction among JMJD3 and UTX, which may play important roles in maintaining endoplasmic reticulum (ER) homeostasis in tumor cells. Interestingly, our clinical data analysis showed that high expression of JMJD3 and UTX was associated with T stage and worse prognosis of ESCC patients, further supporting the importance of the above findings. In conclusion, our findings suggest that the combination of CuET and targeting JMJD3/UTX may be a safe, effective, and available treatment for ESCC. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism and Drug Targets)
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17 pages, 3589 KiB  
Article
Metabolic Reprogramming by Ribitol Expands the Therapeutic Window of BETi JQ1 against Breast Cancer
by Ravi Doddapaneni, Jason D. Tucker, Pei J. Lu and Qi L. Lu
Cancers 2023, 15(17), 4356; https://doi.org/10.3390/cancers15174356 - 1 Sep 2023
Viewed by 1338
Abstract
Many cancer patients still lack effective treatments, and pre-existing or acquired resistance limits the clinical benefit of even the most advanced medicines. Recently, much attention has been given to the role of metabolism in cancer, expanding from the Warburg effect to highlight unique [...] Read more.
Many cancer patients still lack effective treatments, and pre-existing or acquired resistance limits the clinical benefit of even the most advanced medicines. Recently, much attention has been given to the role of metabolism in cancer, expanding from the Warburg effect to highlight unique patterns that, in turn, may improve diagnostic and therapeutic approaches. Our recent metabolomics study revealed that ribitol can alter glycolysis in breast cancer cells. In the current study, we investigate the combinatorial effects of ribitol with several other anticancer drugs (chrysin, lonidamine, GSK2837808A, CB-839, JQ1, and shikonin) in various breast cancer cells (MDA-MB-231, MCF-7, and T-47D). The combination of ribitol with JQ1 synergistically inhibited the proliferation and migration of breast cancer cells cell-type dependently, only observed in the triple-negative MDA-MB-231 breast cancer cells. This synergy is associated with the differential effects of the 2 compounds on expression of the genes involved in cell survival and death, specifically downregulation in c-Myc and other anti-apoptotic proteins (Bcl-2, Bcl-xL, Mcl-1), but upregulation in p53 and cytochrome C levels. Glycolysis is differentially altered, with significant downregulation of glucose-6-phosphate and lactate by ribitol and JQ1, respectively. The overall effect of the combined treatment on metabolism and apoptosis-related genes results in significant synergy in the inhibition of cell growth and induction of apoptosis. Given the fact that ribitol is a metabolite with limited side effects, a combined therapy is highly desirable with relative ease to apply in the clinic for treating an appropriate cancer population. Our results also emphasize that, similar to traditional drug development, the therapeutic potential of targeting metabolism for cancer treatment may only be achieved in combination with other drugs and requires the identification of a specific cancer population. The desire to apply metabolomic intervention to a large scope of cancer types may be one of the reasons identification of this class of drugs in a clinical trial setting has been delayed. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism and Drug Targets)
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