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Tumor Metabolism and Signaling
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Tumor Metabolism and Signaling

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

Deadline for manuscript submissions: closed (30 April 2021) | Viewed by 10089

Special Issue Editor

Dr. Niramol Savaraj

E-Mail Website
Guest Editor
Department of Medicine, University of Miami Miller School of Medicine, Miami, FL, USA
Interests: biochemistry; genetics and molecular biology; tumor metabolism and signaling

Special Issue Information

Dear Colleagues,

Cancer cells are known to possess extraordinary capability to expand and survive in the harsh environment.   In order to do so, they use a number of metabolic reprogramming to ensure both fuel and building block supplies are sufficient. In fact, most tumor cells utilize “aerobic glycolysis”, the so called “Warburg effect” to generate sufficient ATP and nucleotides.  In addition, they also require amino acids to sustain their proliferation. The key amino acids which are essential for tumor cells to multiply and invade are glutamine, arginine, leucine and serine.  Tumor cells are also surrounded by immune cells, macrophages, leukocytes and fibroblasts which also require nutrients to survive and eliminate tumor cells. Thus, the dynamic between tumor cells and stromal cells/immune cells is important to determine the growth and survival of tumor cells. Tumor and immune cells /stromal cells metabolism play an important role in this process. In this issue, we plan to discuss the key aspects in tumor metabolism and signaling and how to exploit them for treatment.

Dr. Niramol Savaraj
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. 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.

Published Papers (3 papers)

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Review

18 pages, 841 KiB  
Review
Enhancing the Effect of Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand Signaling and Arginine Deprivation in Melanoma
by Chunjing Wu, Min You, Dao Nguyen, Medhi Wangpaichitr, Ying-Ying Li, Lynn G. Feun, Macus T. Kuo and Niramol Savaraj
Int. J. Mol. Sci. 2021, 22(14), 7628; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147628 - 16 Jul 2021
Cited by 5 | Viewed by 2312
Abstract
Melanoma as a very aggressive type of cancer is still in urgent need of improved treatment. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and arginine deiminase (ADI-PEG20) are two of many suggested drugs for treating melanoma. Both have shown anti-tumor activities without harming normal [...] Read more.
Melanoma as a very aggressive type of cancer is still in urgent need of improved treatment. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and arginine deiminase (ADI-PEG20) are two of many suggested drugs for treating melanoma. Both have shown anti-tumor activities without harming normal cells. However, resistance to both drugs has also been noted. Studies on the mechanism of action of and resistance to these drugs provide multiple targets that can be utilized to increase the efficacy and overcome the resistance. As a result, combination strategies have been proposed for these drug candidates with various other agents, and achieved enhanced or synergistic anti-tumor effect. The combination of TRAIL and ADI-PEG20 as one example can greatly enhance the cytotoxicity to melanoma cells including those resistant to the single component of this combination. It is found that combination treatment generally can alter the expression of the components of cell signaling in melanoma cells to favor cell death. In this paper, the signaling of TRAIL and ADI-PEG20-induced arginine deprivation including the main mechanism of resistance to these drugs and exemplary combination strategies is discussed. Finally, factors hampering the clinical application of both drugs, current and future development to overcome these hurdles are briefly discussed. Full article
(This article belongs to the Special Issue Tumor Metabolism and Signaling)
22 pages, 1585 KiB  
Review
Cisplatin Resistance and Redox-Metabolic Vulnerability: A Second Alteration
by Medhi Wangpaichitr, George Theodoropoulos, Dan J. M. Nguyen, Chunjing Wu, Sydney A. Spector, Lynn G. Feun and Niramol Savaraj
Int. J. Mol. Sci. 2021, 22(14), 7379; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22147379 - 09 Jul 2021
Cited by 14 | Viewed by 3508
Abstract
The development of drug resistance in tumors is a major obstacle to effective cancer chemotherapy and represents one of the most significant complications to improving long-term patient outcomes. Despite early positive responsiveness to platinum-based chemotherapy, the majority of lung cancer patients develop resistance. [...] Read more.
The development of drug resistance in tumors is a major obstacle to effective cancer chemotherapy and represents one of the most significant complications to improving long-term patient outcomes. Despite early positive responsiveness to platinum-based chemotherapy, the majority of lung cancer patients develop resistance. The development of a new combination therapy targeting cisplatin-resistant (CR) tumors may mark a major improvement as salvage therapy in these patients. The recent resurgence in research into cellular metabolism has again confirmed that cancer cells utilize aerobic glycolysis (“the Warburg effect”) to produce energy. Hence, this observation still remains a characteristic hallmark of altered metabolism in certain cancer cells. However, recent evidence promotes another concept wherein some tumors that acquire resistance to cisplatin undergo further metabolic alterations that increase tumor reliance on oxidative metabolism (OXMET) instead of glycolysis. Our review focuses on molecular changes that occur in tumors due to the relationship between metabolic demands and the importance of NAD+ in redox (ROS) metabolism and the crosstalk between PARP-1 (Poly (ADP ribose) polymerase-1) and SIRTs (sirtuins) in CR tumors. Finally, we discuss a role for the tumor metabolites of the kynurenine pathway (tryptophan catabolism) as effectors of immune cells in the tumor microenvironment during acquisition of resistance in CR cells. Understanding these concepts will form the basis for future targeting of CR cells by exploiting redox-metabolic changes and their consequences on immune cells in the tumor microenvironment as a new approach to improve overall therapeutic outcomes and survival in patients who fail cisplatin. Full article
(This article belongs to the Special Issue Tumor Metabolism and Signaling)
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16 pages, 912 KiB  
Review
Connecting Cholesterol Efflux Factors to Lung Cancer Biology and Therapeutics
by Maria Maslyanko, Ryan D. Harris and David Mu
Int. J. Mol. Sci. 2021, 22(13), 7209; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22137209 - 05 Jul 2021
Cited by 5 | Viewed by 3525
Abstract
Cholesterol is a foundational molecule of biology. There is a long-standing interest in understanding how cholesterol metabolism is intertwined with cancer biology. In this review, we focus on the known connections between lung cancer and molecules mediating cholesterol efflux. A major take-home lesson [...] Read more.
Cholesterol is a foundational molecule of biology. There is a long-standing interest in understanding how cholesterol metabolism is intertwined with cancer biology. In this review, we focus on the known connections between lung cancer and molecules mediating cholesterol efflux. A major take-home lesson is that the roles of many cholesterol efflux factors remain underexplored. It is our hope that this article would motivate others to investigate how cholesterol efflux factors contribute to lung cancer biology. Full article
(This article belongs to the Special Issue Tumor Metabolism and Signaling)
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