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The Role of Cell Metabolism in Cancer
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The Role of Cell Metabolism in Cancer

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

Deadline for manuscript submissions: closed (15 January 2023) | Viewed by 15324

Special Issue Editors

Dr. Yao-An Shen

E-Mail Website
Guest Editor
Department of Pathology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan
Interests: translational research; cell therapy; cancer metabolism; cancer stem cell research; induced pluripotent stem cell research; nanomedicine
Dr. Sérgio Dias

E-Mail Website
Co-Guest Editor
University of Lisbon Faculty of Medicine, Institute of Molecular Medicine, Lisbon, Portugal
Interests: breast cancer; immunology; leukemia; miRNA

Special Issue Information

Dear Colleagues, 

This Special Issue is designed to provide information on the latest advances in cancer metabolism. Instead of living solitary, cancer cells are surrounded by a complex ecosystem of extracellular matrix, immune cells, endothelial cells, and cancer-associated fibroblasts. Cancer stem cells (CSCs), unlike differentiated tumor progenies, undergo metabolic reprogramming and, depending on the type of cancer, rely on glycolysis, glutaminolysis, or fatty acids for survival. Because of their metabolic flexibility, CSCs can switch between distinct metabolisms for tumor progression in a diversity of microenvironments and develop therapeutic resistance. Metabolic interventions could be combined with standard cytotoxic regimens to prevent recurrence and metastasis and achieve more effective long-term disease remission. For this Special Issue, we invite the submission of research articles and reviews from basic, translational, and preclinical research. We aim to gather new perspectives on the role of cell metabolism in cancer biology and to focus on emerging tactics that highlight mitochondrial targeting in the context of cancer treatment.

Dr. Yao-An Shen
Dr. Sérgio Dias
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
  • cancer stem cell
  • metabolomics
  • mitophagy
  • metabolic plasticity
  • therapeutic resistance
  • metastasis
  • tumor microenvironment
  • immune cells
  • drug development

Published Papers (6 papers)

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Research

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15 pages, 5259 KiB  
Article
Anticancer Study of a Novel Pan-HDAC Inhibitor MPT0G236 in Colorectal Cancer Cells
by Feng-Lung Tsai, Han-Li Huang, Mei-Jung Lai, Jing-Ping Liou, Shiow-Lin Pan and Chia-Ron Yang
Int. J. Mol. Sci. 2023, 24(16), 12588; https://doi.org/10.3390/ijms241612588 - 9 Aug 2023
Viewed by 1398
Abstract
Colorectal cancer (CRC) is one of the most commonly diagnosed malignancies and a leading cause of cancer worldwide. Histone deacetylases (HDACs), which regulate cell proliferation and survival, are associated with the development and progression of cancer. Moreover, HDAC inhibitors are promising therapeutic targets, [...] Read more.
Colorectal cancer (CRC) is one of the most commonly diagnosed malignancies and a leading cause of cancer worldwide. Histone deacetylases (HDACs), which regulate cell proliferation and survival, are associated with the development and progression of cancer. Moreover, HDAC inhibitors are promising therapeutic targets, with five HDAC inhibitors approved for cancer treatment to date. However, their safety profile necessitates the exploration of well-tolerated HDAC inhibitors that can be used in cancer therapeutic strategies. In this study, the pan-HDAC inhibitor MPT0G236 reduced the viability and inhibited the proliferation of human colorectal cancer cells, and normal human umbilical vein endothelial cells (HUVECs) showed reduced sensitivity. These findings indicated that MPT0G236 specifically targeted malignant tumor cells. Notably, MPT0G236 significantly inhibited the activities of HDAC1, HDAC2, and HDAC3, Class I HDACs, as well as HDAC6, a Class IIb HDAC, at low nanomolar concentrations. Additionally, it promoted the accumulation of acetyl-α-tubulin and acetyl-histone H3 in HCT-116 and HT-29 cells in a concentration-dependent manner. Furthermore, MPT0G236 treatment induced G2/M cell cycle arrest in CRC cells by initially regulating the levels of cell-cycle-related proteins, such as p-MPM2; specifically reducing p-cdc2 (Y15), cyclin B1, and cdc25C levels; and subsequently inducing apoptosis through the caspase-dependent pathways and PARP activation. Our findings demonstrate that MPT0G236 exhibits significant anticancer activity in human colorectal cancer cells. Full article
(This article belongs to the Special Issue The Role of Cell Metabolism in Cancer)
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15 pages, 2103 KiB  
Article
Mebendazole Increases Anticancer Activity of Radiotherapy in Radiotherapy-Resistant Triple-Negative Breast Cancer Cells by Enhancing Natural Killer Cell-Mediated Cytotoxicity
by Hoon Sik Choi, Young Shin Ko, Hana Jin, Ki Mun Kang, In Bong Ha, Hojin Jeong, Jeong-hee Lee, Bae Kwon Jeong and Hye Jung Kim
Int. J. Mol. Sci. 2022, 23(24), 15493; https://doi.org/10.3390/ijms232415493 - 7 Dec 2022
Cited by 4 | Viewed by 2508
Abstract
Breast cancer is the most commonly diagnosed cancer worldwide and ranks first in terms of both prevalence and cancer-related mortality in women. In this study, we aimed to evaluate the anticancer effect of mebendazole (MBZ) and radiotherapy (RT) concomitant use in triple-negative breast [...] Read more.
Breast cancer is the most commonly diagnosed cancer worldwide and ranks first in terms of both prevalence and cancer-related mortality in women. In this study, we aimed to evaluate the anticancer effect of mebendazole (MBZ) and radiotherapy (RT) concomitant use in triple-negative breast cancer (TNBC) cells and elucidate the underlying mechanisms of action. Breast cancer mouse models and several types of breast cancer cells, including TNBC-derived RT-resistant (RT-R) MDA-MB-231 cells, were treated with MBZ and/or RT. In mice, changes in body weight, renal and liver toxicity, tumor volume, and number of lung metastases were determined. In cells, cell viability, colony formation, scratch wound healing, Matrigel invasion, and protein expression using western blotting were determined. Our findings showed that MBZ and RT combined treatment increased the anticancer effect of RT without additional toxicity. In addition, we noted that cyclin B1, PH2AX, and natural killer (NK) cell-mediated cytotoxicity increased following MBZ + RT treatment compared to unaided RT. Our results suggest that MBZ + RT have an enhanced anticancer effect in TNBC which acquires radiation resistance through blocking cell cycle progression, initiating DNA double-strand breaks, and promoting NK cell-mediated cytotoxicity. Full article
(This article belongs to the Special Issue The Role of Cell Metabolism in Cancer)
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20 pages, 7813 KiB  
Article
A New Chemotactic Mechanism Governs Long-Range Angiogenesis Induced by Patching an Arterial Graft into a Vein
by Dhisa Minerva, Nuha Loling Othman, Takashi Nakazawa, Yukinobu Ito, Makoto Yoshida, Akiteru Goto and Takashi Suzuki
Int. J. Mol. Sci. 2022, 23(19), 11208; https://doi.org/10.3390/ijms231911208 - 23 Sep 2022
Cited by 1 | Viewed by 1514
Abstract
Chemotaxis, the migration of cells in response to chemical stimulus, is an important concept in the angiogenesis model. In most angiogenesis models, chemotaxis is defined as the migration of a sprout tip in response to the upgradient of the VEGF (vascular endothelial growth [...] Read more.
Chemotaxis, the migration of cells in response to chemical stimulus, is an important concept in the angiogenesis model. In most angiogenesis models, chemotaxis is defined as the migration of a sprout tip in response to the upgradient of the VEGF (vascular endothelial growth factor). However, we found that angiogenesis induced by performing arterial patch grafting on rabbits occurred under the decreasing VEGFA gradient. Data show that the VEGFA concentration peaked at approximately 0.3 to 0.5 cm away from the arterial patch and decreased as the measurement approaches the patch. We also observed that the new blood vessels formed are twisted and congested in some areas, in a distinguishable manner from non-pathological blood vessels. To explain these observations, we developed a mathematical model and compared the results from numerical simulations with the experimental data. We introduced a new chemotactic velocity using the temporal change in the chemoattractant gradient to govern the sprout tip migration. We performed a hybrid simulation to illustrate the growth of new vessels. Results indicated the speed of growth of new vessels oscillated before reaching the periphery of the arterial patch. Crowded and congested blood vessel formation was observed during numerical simulations. Thus, our numerical simulation results agreed with the experimental data. Full article
(This article belongs to the Special Issue The Role of Cell Metabolism in Cancer)
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Review

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16 pages, 1338 KiB  
Review
Metabolic Rewiring in Adult-Type Diffuse Gliomas
by Jong-Whi Park
Int. J. Mol. Sci. 2023, 24(8), 7348; https://doi.org/10.3390/ijms24087348 - 16 Apr 2023
Cited by 1 | Viewed by 1677
Abstract
Multiple metabolic pathways are utilized to maintain cellular homeostasis. Given the evidence that altered cell metabolism significantly contributes to glioma biology, the current research efforts aim to improve our understanding of metabolic rewiring between glioma’s complex genotype and tissue context. In addition, extensive [...] Read more.
Multiple metabolic pathways are utilized to maintain cellular homeostasis. Given the evidence that altered cell metabolism significantly contributes to glioma biology, the current research efforts aim to improve our understanding of metabolic rewiring between glioma’s complex genotype and tissue context. In addition, extensive molecular profiling has revealed activated oncogenes and inactivated tumor suppressors that directly or indirectly impact the cellular metabolism that is associated with the pathogenesis of gliomas. The mutation status of isocitrate dehydrogenases (IDHs) is one of the most important prognostic factors in adult-type diffuse gliomas. This review presents an overview of the metabolic alterations in IDH-mutant gliomas and IDH-wildtype glioblastoma (GBM). A particular focus is placed on targeting metabolic vulnerabilities to identify new therapeutic strategies for glioma. Full article
(This article belongs to the Special Issue The Role of Cell Metabolism in Cancer)
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17 pages, 1635 KiB  
Review
Targeting Mitochondrial Metabolic Reprogramming as a Potential Approach for Cancer Therapy
by Liufeng Zhang, Yuancheng Wei, Shengtao Yuan and Li Sun
Int. J. Mol. Sci. 2023, 24(5), 4954; https://doi.org/10.3390/ijms24054954 - 4 Mar 2023
Cited by 11 | Viewed by 3585
Abstract
Abnormal energy metabolism is a characteristic of tumor cells, and mitochondria are important components of tumor metabolic reprogramming. Mitochondria have gradually received the attention of scientists due to their important functions, such as providing chemical energy, producing substrates for tumor anabolism, controlling REDOX [...] Read more.
Abnormal energy metabolism is a characteristic of tumor cells, and mitochondria are important components of tumor metabolic reprogramming. Mitochondria have gradually received the attention of scientists due to their important functions, such as providing chemical energy, producing substrates for tumor anabolism, controlling REDOX and calcium homeostasis, participating in the regulation of transcription, and controlling cell death. Based on the concept of reprogramming mitochondrial metabolism, a range of drugs have been developed to target the mitochondria. In this review, we discuss the current progress in mitochondrial metabolic reprogramming and summarized the corresponding treatment options. Finally, we propose mitochondrial inner membrane transporters as new and feasible therapeutic targets. Full article
(This article belongs to the Special Issue The Role of Cell Metabolism in Cancer)
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20 pages, 1295 KiB  
Review
Therapeutic Targeting of Glutaminolysis as a Novel Strategy to Combat Cancer Stem Cells
by Ting-Wan Kao, Yao-Chen Chuang, Hsin-Lun Lee, Chia-Chun Kuo and Yao-An Shen
Int. J. Mol. Sci. 2022, 23(23), 15296; https://doi.org/10.3390/ijms232315296 - 4 Dec 2022
Cited by 7 | Viewed by 3935
Abstract
Rare subpopulations of cancer stem cells (CSCs) have the ability to self-renew and are the primary driving force behind cancer metastatic dissemination and the preeminent hurdle to cancer treatment. As opposed to differentiated, non-malignant tumor offspring, CSCs have sophisticated metabolic patterns that, depending [...] Read more.
Rare subpopulations of cancer stem cells (CSCs) have the ability to self-renew and are the primary driving force behind cancer metastatic dissemination and the preeminent hurdle to cancer treatment. As opposed to differentiated, non-malignant tumor offspring, CSCs have sophisticated metabolic patterns that, depending on the kind of cancer, rely mostly on the oxidation of major fuel substrates such as glucose, glutamine, and fatty acids for survival. Glutaminolysis is a series of metabolic reactions that convert glutamine to glutamate and, eventually, α-ketoglutarate, an intermediate in the tricarboxylic acid (TCA) cycle that provides biosynthetic building blocks. These building blocks are mostly utilized in the synthesis of macromolecules and antioxidants for redox homeostasis. A recent study revealed the cellular and molecular interconnections between glutamine and cancer stemness in the cell. Researchers have increasingly focused on glutamine catabolism in their attempt to discover an effective therapy for cancer stem cells. Targeting catalytic enzymes in glutaminolysis, such as glutaminase (GLS), is achievable with small molecule inhibitors, some of which are in early-phase clinical trials and have promising safety profiles. This review summarizes the current findings in glutaminolysis of CSCs and focuses on novel cancer therapies that target glutaminolysis in CSCs. Full article
(This article belongs to the Special Issue The Role of Cell Metabolism in Cancer)
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