Cancer Cell Metabolism (2nd Edition)

Topic Information

Dear Colleagues,

In recent years, we have seen an enormous increase in studies associated with cancer metabolism. Cancer metabolism can refer to all types of alterations in the metabolic pathways that are evident in cancer cells compared with non-malignant cells of the same tissue. Metabolic alterations in cancer cells are numerous and include aerobic glycolysis, reduced oxidative phosphorylation, and the increased generation of biosynthetic intermediates needed for cell proliferation and survival. Furthermore, metabolic rewiring can support common cancer features such as migration, invasion, and metastasis. With the many discoveries made in the past decade, we now realize that cancer metabolism is a key component of cellular transformation. However, emerging evidence also indicates that cancer metabolism is complex, and further studies are needed to apply our knowledge to therapeutic settings. For this Special Issue, we invite authors to submit contributions that provide novel findings in the field of cancer metabolism. We welcome results from basic research, preclinical, or clinical research and reviews that highlight new findings in the field of cancer metabolism.

Prof. Dr. Arun Dharmarajan
Prof. Dr. Paula Guedes De Pinho
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Cancers cancers	5.2	7.4	2009	17.9 Days	CHF 2900	Submit
Cells cells	6.0	9.0	2012	16.6 Days	CHF 2700	Submit
Endocrines endocrines	-	-	2020	27.2 Days	CHF 1000	Submit
International Journal of Molecular Sciences ijms	5.6	7.8	2000	16.3 Days	CHF 2900	Submit
Metabolites metabolites	4.1	5.3	2011	13.2 Days	CHF 2700	Submit

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Published Papers (5 papers)

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All Cancers Cells Endocrines IJMS Metabolites

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48 pages, 5245 KiB  

Open AccessReview

Metabolic Roles of HIF1, c-Myc, and p53 in Glioma Cells

by Cristina Trejo-Solís, Rosa Angélica Castillo-Rodríguez, Norma Serrano-García, Daniela Silva-Adaya, Salvador Vargas-Cruz, Elda Georgina Chávez-Cortéz, Juan Carlos Gallardo-Pérez, Sergio Zavala-Vega, Arturo Cruz-Salgado and Roxana Magaña-Maldonado

Metabolites 2024, 14(5), 249; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo14050249 - 25 Apr 2024

Viewed by 251

Abstract

The metabolic reprogramming that promotes tumorigenesis in glioblastoma is induced by dynamic alterations in the hypoxic tumor microenvironment, as well as in transcriptional and signaling networks, which result in changes in global genetic expression. The signaling pathways PI3K/AKT/mTOR and RAS/RAF/MEK/ERK stimulate cell metabolism, [...] Read more.

The metabolic reprogramming that promotes tumorigenesis in glioblastoma is induced by dynamic alterations in the hypoxic tumor microenvironment, as well as in transcriptional and signaling networks, which result in changes in global genetic expression. The signaling pathways PI3K/AKT/mTOR and RAS/RAF/MEK/ERK stimulate cell metabolism, either directly or indirectly, by modulating the transcriptional factors p53, HIF1, and c-Myc. The overexpression of HIF1 and c-Myc, master regulators of cellular metabolism, is a key contributor to the synthesis of bioenergetic molecules that mediate glioma cell transformation, proliferation, survival, migration, and invasion by modifying the transcription levels of key gene groups involved in metabolism. Meanwhile, the tumor-suppressing protein p53, which negatively regulates HIF1 and c-Myc, is often lost in glioblastoma. Alterations in this triad of transcriptional factors induce a metabolic shift in glioma cells that allows them to adapt and survive changes such as mutations, hypoxia, acidosis, the presence of reactive oxygen species, and nutrient deprivation, by modulating the activity and expression of signaling molecules, enzymes, metabolites, transporters, and regulators involved in glycolysis and glutamine metabolism, the pentose phosphate cycle, the tricarboxylic acid cycle, and oxidative phosphorylation, as well as the synthesis and degradation of fatty acids and nucleic acids. This review summarizes our current knowledge on the role of HIF1, c-Myc, and p53 in the genic regulatory network for metabolism in glioma cells, as well as potential therapeutic inhibitors of these factors. Full article

(This article belongs to the Topic Cancer Cell Metabolism (2nd Edition))

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20 pages, 3482 KiB  

Open AccessReview

The Emerging Role of LPA as an Oncometabolite

by Theodoros Karalis and George Poulogiannis

Cells 2024, 13(7), 629; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13070629 - 04 Apr 2024

Viewed by 657

Abstract

Lysophosphatidic acid (LPA) is a phospholipid that displays potent signalling activities that are regulated in both an autocrine and paracrine manner. It can be found both extra- and intracellularly, where it interacts with different receptors to activate signalling pathways that regulate a plethora [...] Read more.

Lysophosphatidic acid (LPA) is a phospholipid that displays potent signalling activities that are regulated in both an autocrine and paracrine manner. It can be found both extra- and intracellularly, where it interacts with different receptors to activate signalling pathways that regulate a plethora of cellular processes, including mitosis, proliferation and migration. LPA metabolism is complex, and its biosynthesis and catabolism are under tight control to ensure proper LPA levels in the body. In cancer patient specimens, LPA levels are frequently higher compared to those of healthy individuals and often correlate with poor responses and more aggressive disease. Accordingly, LPA, through promoting cancer cell migration and invasion, enhances the metastasis and dissemination of tumour cells. In this review, we summarise the role of LPA in the regulation of critical aspects of tumour biology and further discuss the available pre-clinical and clinical evidence regarding the feasibility and efficacy of targeting LPA metabolism for effective anticancer therapy. Full article

(This article belongs to the Topic Cancer Cell Metabolism (2nd Edition))

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23 pages, 1881 KiB  

Open AccessReview

Targeting Dysregulated Lipid Metabolism in Cancer with Pharmacological Inhibitors

by Amogh Gupta, Dipanwita Das and Reshma Taneja

Cancers 2024, 16(7), 1313; https://0-doi-org.brum.beds.ac.uk/10.3390/cancers16071313 - 28 Mar 2024

Viewed by 690

Abstract

Metabolic plasticity is recognised as a hallmark of cancer cells, enabling adaptation to microenvironmental changes throughout tumour progression. A dysregulated lipid metabolism plays a pivotal role in promoting oncogenesis. Oncogenic signalling pathways, such as PI3K/AKT/mTOR, JAK/STAT, Hippo, and NF-kB, intersect with the lipid [...] Read more.

Metabolic plasticity is recognised as a hallmark of cancer cells, enabling adaptation to microenvironmental changes throughout tumour progression. A dysregulated lipid metabolism plays a pivotal role in promoting oncogenesis. Oncogenic signalling pathways, such as PI3K/AKT/mTOR, JAK/STAT, Hippo, and NF-kB, intersect with the lipid metabolism to drive tumour progression. Furthermore, altered lipid signalling in the tumour microenvironment contributes to immune dysfunction, exacerbating oncogenesis. This review examines the role of lipid metabolism in tumour initiation, invasion, metastasis, and cancer stem cell maintenance. We highlight cybernetic networks in lipid metabolism to uncover avenues for cancer diagnostics, prognostics, and therapeutics. Full article

(This article belongs to the Topic Cancer Cell Metabolism (2nd Edition))

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15 pages, 5569 KiB  

Open AccessArticle

Metabolic Responses of Lung Adenocarcinoma Cells to Survive under Stressful Conditions Associated with Tumor Microenvironment

by Angeles Carlos-Reyes, Susana Romero-Garcia and Heriberto Prado-Garcia

Metabolites 2024, 14(2), 103; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo14020103 - 02 Feb 2024

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Abstract

Solid tumors frequently present a heterogeneous tumor microenvironment. Because tumors have the potential to proliferate quickly, the consequence is a reduction in the nutrients, a reduction in the pH (<6.8), and a hypoxic environment. Although it is often assumed that tumor clones show [...] Read more.

Solid tumors frequently present a heterogeneous tumor microenvironment. Because tumors have the potential to proliferate quickly, the consequence is a reduction in the nutrients, a reduction in the pH (<6.8), and a hypoxic environment. Although it is often assumed that tumor clones show a similar growth rate with little variations in nutrient consumption, the present study shows how growth-specific rate (µ), the specific rates of glucose, lactate, and glutamine consumption (qS), and the specific rates of lactate and glutamate production (qP) of 2D-cultured lung tumor cells are affected by changes in their environment. We determined in lung tumor cells (A427, A549, Calu-1, and SKMES-1) the above mentioned kinetic parameters during the exponential phase under different culture conditions, varying the predominant carbon source, pH, and oxygen tension. MCF-7 cells, a breast tumor cell line that can consume lactate, and non-transformed fibroblast cells (MRC-5) were included as controls. We also analyzed how cell-cycle progression and the amino acid transporter CD98 expression were affected. Our results show that: (1) In glucose presence, μ increased, but q_{S Glucose} and q_{P Lactate} decreased when tumor cells were cultured under acidosis as opposed to neutral conditions; (2) most lung cancer cell lines consumed lactate under normoxia or hypoxia; (3) although q_{S Glutamine} diminished under hypoxia or acidosis, it slightly increased in lactate presence, a finding that was associated with CD98 upregulation; and (4) under acidosis, G0/G1 arrest was induced in A427 cancer cells, although this phenomenon was significantly increased when glucose was changed by lactate as the predominant carbon-source. Hence, our results provide an understanding of metabolic responses that tumor cells develop to survive under stressful conditions, providing clues for developing promising opportunities to improve traditional cancer therapies. Full article

(This article belongs to the Topic Cancer Cell Metabolism (2nd Edition))

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17 pages, 3562 KiB  

Open AccessArticle

Modulation of Cisplatin Sensitivity through TRPML1-Mediated Lysosomal Exocytosis in Ovarian Cancer Cells: A Comprehensive Metabolomic Approach

by Boyun Kim, Gaeun Kim, Heeyeon Kim, Yong Sang Song and Jewon Jung

Cells 2024, 13(2), 115; https://0-doi-org.brum.beds.ac.uk/10.3390/cells13020115 - 08 Jan 2024

Cited by 4 | Viewed by 1214

Abstract

Background: The lysosome has emerged as a promising target for overcoming chemoresistance, owing to its role in facilitating the lysosomal sequestration of drugs. The lysosomal calcium channel TRPML1 not only influences lysosomal biogenesis but also coordinates both endocytosis and exocytosis. This study explored [...] Read more.

Background: The lysosome has emerged as a promising target for overcoming chemoresistance, owing to its role in facilitating the lysosomal sequestration of drugs. The lysosomal calcium channel TRPML1 not only influences lysosomal biogenesis but also coordinates both endocytosis and exocytosis. This study explored the modulation of cisplatin sensitivity by regulating TRPML1-mediated lysosomal exocytosis and identified the metabolomic profile altered by TRPML1 inhibition. Methods: We used four types of ovarian cancer cells: two cancer cell lines (OVCAR8 and TOV21G) and two patient-derived ovarian cancer cells. Metabolomic analyses were conducted to identify altered metabolites by TRPML1 inhibition. Results: Lysosomal exocytosis in response to cisplatin was observed in resistant cancer cells, whereas the phenomenon was absent in sensitive cancer cells. Through the pharmacological intervention of TRPML1, lysosomal exocytosis was interrupted, leading to the sensitization of resistant cancer cells to cisplatin treatment. To assess the impact of lysosomal exocytosis on chemoresistance, we conducted an untargeted metabolomic analysis on cisplatin-resistant ovarian cancer cells with TRPML1 inhibition. Among the 1446 differentially identified metabolites, we focused on 84 significant metabolites. Metabolite set analysis revealed their involvement in diverse pathways. Conclusions: These findings collectively have the potential to enhance our understanding of the interplay between lysosomal exocytosis and chemoresistance, providing valuable insights for the development of innovative therapeutic strategies. Full article

(This article belongs to the Topic Cancer Cell Metabolism (2nd Edition))

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