ijms-logo

Journal Browser

Journal Browser

Special Issue "Cancer Cell Metabolism—Pathways and Biology"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 May 2019).

Special Issue Editors

Prof. Dr. Maria Shoshan
E-Mail Website
Guest Editor
Department of Oncology-Pathology, Karolinska Institute, 171 76 Stockholm, Sweden
Tel. +46 8 51775460
Interests: the roles of altered cancer cell metabolism in chemoresistance and tumor progression; the metabolism of cancer stem cells; in ovarian cancer, the roles of cytokine/adipokine interactions between cancer cells and adipocytes; cancer cell metabolism; chemoresistance; tumor progression; cancer stem cells (tumor-initiating cells, TICs); adipocytes and adipokines; tumor microenvironment
Prof. Dr. Valdemar Máximo
E-Mail Website1 Website2
Guest Editor
Cancer Signaling and Metabolism Research Group, Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), Porto, Portugal
Interests: cancer signaling; cancer metabolism

Special Issue Information

Dear Colleagues,

With recent insights into cancer cell metabolism, our already complex perception of cancer biology has acquired several new layers of complexity. The foci of molecular cancer research have expanded from genomics and proteomics to metabolomics, and the renewed interest in the aerobic glycolysis of cancer cells has developed into research on the roles of other sources for catabolism and anabolism. These and other related factors all contribute to the general as well as the specific and malignant properties of cancer cells and tumors and are, therefore, of importance for future diagnostics and treatment strategies. The extent of research interest in cancer cell metabolism is reflected in a PubMed search (May 2018) which yielded 111 reviews on this subject, only in the last five years. It is thus likely that much of the basic concepts and models are already adequately covered in these reviews. In this Special Issue, in order to go beyond these, we hope to provide brief background summaries, as well as some novel models and some examples, of how clinically-oriented research may reflect or apply molecular findings.

This Special Issue welcomes both original papers and review articles addressing one or several of the above-mentioned issues, or of the topics mentioned in the keywords listed below.

Prof. Dr. Maria Shoshan
Prof. Dr. Valdemar Máximo
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 papers will be 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

  • Overview of fundamentals of cancer cell metabolism
  • Anabolic and catabolic pathways
  • Mitochondrial functions
  • Metabolites and metabolomics in cancer
  • Metabolic plasticity
  • Microenvironment
  • Cancer therapy and resistance
  • Diagnosis and prognosis

Published Papers (5 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

Open AccessArticle
Methionine Adenosyltransferase 1a (MAT1A) Enhances Cell Survival During Chemotherapy Treatment and is Associated with Drug Resistance in Bladder Cancer PDX Mice
Int. J. Mol. Sci. 2019, 20(20), 4983; https://doi.org/10.3390/ijms20204983 - 09 Oct 2019
Abstract
Bladder cancer is among the top ten most common cancers, with about ~380,000 new cases and ~150,000 deaths per year worldwide. Tumor relapse following chemotherapy treatment has long been a significant challenge towards completely curing cancer. We have utilized a patient-derived bladder cancer [...] Read more.
Bladder cancer is among the top ten most common cancers, with about ~380,000 new cases and ~150,000 deaths per year worldwide. Tumor relapse following chemotherapy treatment has long been a significant challenge towards completely curing cancer. We have utilized a patient-derived bladder cancer xenograft (PDX) platform to characterize molecular mechanisms that contribute to relapse following drug treatment in advanced bladder cancer. Transcriptomic profiling of bladder cancer xenograft tumors by RNA-sequencing analysis, before and after relapse, following a 21-day cisplatin/gemcitabine drug treatment regimen identified methionine adenosyltransferase 1a (MAT1A) as one of the significantly upregulated genes following drug treatment. Survey of patient tumor sections confirmed elevated levels of MAT1A in individuals who received chemotherapy. Overexpression of MAT1A in 5637 bladder cancer cells increased tolerance to gemcitabine and stalled cell proliferation rates, suggesting MAT1A upregulation as a potential mechanism by which bladder cancer cells persist in a quiescent state to evade chemotherapy. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism—Pathways and Biology)
Show Figures

Figure 1

Open AccessArticle
Knockdown of the TP53-Induced Glycolysis and Apoptosis Regulator (TIGAR) Sensitizes Glioma Cells to Hypoxia, Irradiation and Temozolomide
Int. J. Mol. Sci. 2019, 20(5), 1061; https://doi.org/10.3390/ijms20051061 - 01 Mar 2019
Abstract
The TP53-induced glycolysis and apoptosis regulator (TIGAR) has been shown to decrease glycolysis, to activate the pentose phosphate pathway, and to provide protection against oxidative damage. Hypoxic regions are considered characteristic of glioblastoma and linked with resistance to current treatment strategies. Here, we [...] Read more.
The TP53-induced glycolysis and apoptosis regulator (TIGAR) has been shown to decrease glycolysis, to activate the pentose phosphate pathway, and to provide protection against oxidative damage. Hypoxic regions are considered characteristic of glioblastoma and linked with resistance to current treatment strategies. Here, we established that LNT-229 glioma cell lines stably expressed shRNA constructs targeting TIGAR, and exposed them to hypoxia, irradiation and temozolomide. The disruption of TIGAR enhanced levels of reactive oxygen species and cell death under hypoxic conditions, as well as the effectiveness of irradiation and temozolomide. In addition, TIGAR was upregulated by HIF-1α. As a component of a complex network, TIGAR contributes to the metabolic adjustments that arise from either spontaneous or therapy-induced changes in tumor microenvironment. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism—Pathways and Biology)
Show Figures

Graphical abstract

Review

Jump to: Research

Open AccessReview
Unappreciated Role of LDHA and LDHB to Control Apoptosis and Autophagy in Tumor Cells
Int. J. Mol. Sci. 2019, 20(9), 2085; https://doi.org/10.3390/ijms20092085 - 27 Apr 2019
Abstract
Tumor cells possess a high metabolic plasticity, which drives them to switch on the anaerobic glycolysis and lactate production when challenged by hypoxia. Among the enzymes mediating this plasticity through bidirectional conversion of pyruvate and lactate, the lactate dehydrogenase A (LDHA) and lactate [...] Read more.
Tumor cells possess a high metabolic plasticity, which drives them to switch on the anaerobic glycolysis and lactate production when challenged by hypoxia. Among the enzymes mediating this plasticity through bidirectional conversion of pyruvate and lactate, the lactate dehydrogenase A (LDHA) and lactate dehydrogenase B (LDHB), are indicated. LDHA has a higher affinity for pyruvate, preferentially converting pyruvate to lactate, and NADH to NAD+ in anaerobic conditions, whereas LDHB possess a higher affinity for lactate, preferentially converting lactate to pyruvate, and NAD+ to NADH, when oxygen is abundant. Apart from the undisputed role of LDHA and LDHB in tumor cell metabolism and adaptation to unfavorable environmental or cellular conditions, these enzymes participate in the regulation of cell death. This review presents the latest progress made in this area on the roles of LDHA and LDHB in apoptosis and autophagy of tumor cells. Several examples of how LDHA and LDHB impact on these processes, as well as possible molecular mechanisms, will be discussed in this article. The information included in this review points to the legitimacy of modulating LDHA and/or LDHB to target tumor cells in the context of human and veterinary medicine. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism—Pathways and Biology)
Show Figures

Figure 1

Open AccessReview
The Crosstalk Between Cell Adhesion and Cancer Metabolism
Int. J. Mol. Sci. 2019, 20(8), 1933; https://doi.org/10.3390/ijms20081933 - 19 Apr 2019
Cited by 2
Abstract
Cancer cells preferentially use aerobic glycolysis over mitochondria oxidative phosphorylation for energy production, and this metabolic reprogramming is currently recognized as a hallmark of cancer. Oncogenic signaling frequently converges with this metabolic shift, increasing cancer cells’ ability to produce building blocks and energy, [...] Read more.
Cancer cells preferentially use aerobic glycolysis over mitochondria oxidative phosphorylation for energy production, and this metabolic reprogramming is currently recognized as a hallmark of cancer. Oncogenic signaling frequently converges with this metabolic shift, increasing cancer cells’ ability to produce building blocks and energy, as well as to maintain redox homeostasis. Alterations in cell–cell and cell–extracellular matrix (ECM) adhesion promote cancer cell invasion, intravasation, anchorage-independent survival in circulation, and extravasation, as well as homing in a distant organ. Importantly, during this multi-step metastatic process, cells need to induce metabolic rewiring, in order to produce the energy needed, as well as to impair oxidative stress. Although the individual implications of adhesion molecules and metabolic reprogramming in cancer have been widely explored over the years, the crosstalk between cell adhesion molecular machinery and metabolic pathways is far from being clearly understood, in both normal and cancer contexts. This review summarizes our understanding about the influence of cell–cell and cell–matrix adhesion in the metabolic behavior of cancer cells, with a special focus concerning the role of classical cadherins, such as Epithelial (E)-cadherin and Placental (P)-cadherin. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism—Pathways and Biology)
Show Figures

Graphical abstract

Open AccessReview
Current Status and Future Prospects of Clinically Exploiting Cancer-specific Metabolism—Why Is Tumor Metabolism Not More Extensively Translated into Clinical Targets and Biomarkers?
Int. J. Mol. Sci. 2019, 20(6), 1385; https://doi.org/10.3390/ijms20061385 - 19 Mar 2019
Cited by 1
Abstract
Tumor cells exhibit a specialized metabolism supporting their superior ability for rapid proliferation, migration, and apoptotic evasion. It is reasonable to assume that the specific metabolic needs of the tumor cells can offer an array of therapeutic windows as pharmacological disturbance may derail [...] Read more.
Tumor cells exhibit a specialized metabolism supporting their superior ability for rapid proliferation, migration, and apoptotic evasion. It is reasonable to assume that the specific metabolic needs of the tumor cells can offer an array of therapeutic windows as pharmacological disturbance may derail the biochemical mechanisms necessary for maintaining the tumor characteristics, while being less important for normally proliferating cells. In addition, the specialized metabolism may leave a unique metabolic signature which could be used clinically for diagnostic or prognostic purposes. Quantitative global metabolic profiling (metabolomics) has evolved over the last two decades. However, despite the technology’s present ability to measure 1000s of endogenous metabolites in various clinical or biological specimens, there are essentially no examples of metabolomics investigations being translated into actual utility in the cancer clinic. This review investigates the current efforts of using metabolomics as a tool for translation of tumor metabolism into the clinic and further seeks to outline paths for increasing the momentum of using tumor metabolism as a biomarker and drug target opportunity. Full article
(This article belongs to the Special Issue Cancer Cell Metabolism—Pathways and Biology)
Show Figures

Figure 1

Back to TopTop