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Metabolites
Special Issues
Cell Death and Cancer Metabolism
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Cell Death and Cancer Metabolism

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (31 July 2025) | Viewed by 2059

Special Issue Editor

Dr. Zhengrong Yuan

E-Mail Website
Guest Editor
College of Biological Sciences and Technology, Beijing Forestry University, Beijing, China
Interests: bioinformatics; metabolomics; multi-omics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the course of exploring the field of life sciences, the interaction between cancer and metabolism is particularly important and at the forefront of research. Our upcoming Special Issue looks at the mechanisms by which tumors adjust their metabolic networks to support growth, spread, and avoid death, providing new insights into cancer development, progression, and treatment strategies. Cancer cells reshape metabolic pathways to meet their need for energy and biosynthetic precursors, which is not only key to their survival but also opens up new avenues for treatment. With a deeper understanding of these metabolic regulations and their role in cancer development, new areas of research and treatment possibilities are emerging.

This Special Issue of Metabolites will delve into tumor-related metabolic changes and their importance in cancer occurrence, progression, and treatment. Given that the interaction between tumors and metabolism occupies a crucial place in research, we invite colleagues working on how tumors adapt and promote their growth by altering metabolic pathways to contribute. In addition, we will explore the possibility of metabolic targeting strategies against cancer and how metabolic biomarkers can be used to monitor treatment progress.

The Special Issue is also open to research submissions from the field of epidemiology, especially those that reveal the relationship between metabolic factors and cancer risk. With the development of new measurement techniques, bioinformatics tools, and data analysis methods, we are interested in innovative work in these areas.

By focusing on the interaction between cancer and metabolism, we expect this Special Issue to promote a deeper understanding of cancer metabolic pathways and inspire new treatment strategies to effectively address this global health challenge.

Your participation and contribution are highly appreciated.

Dr. Zhengrong Yuan
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. Metabolites is an international peer-reviewed open access monthly 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 2700 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

  • cancer metabolism
  • metabolic reprogramming
  • tumor growth
  • metabolic biomarkers
  • therapeutic strategies
  • metabolic regulation
  • cancer treatment

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Published Papers (2 papers)

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17 pages, 4907 KB  
Article
Uncovering Anticancer Mechanisms of Spiramycin Derivatives Using Transcriptomic and Metabolomic Analyses
by Renyu Yang, Wuxiyar Otkur, Tingze Feng, Yirong Li, Shaojun Pei, Huan Qi, Yaopeng Zhao, Yao Lu and Hailong Piao
Metabolites 2025, 15(10), 647; https://doi.org/10.3390/metabo15100647 - 27 Sep 2025
Viewed by 353
Abstract
Background: Carrimycin is a mixture of spiramycin derivatives with antibacterial functions. However, recent studies have shown that it possesses certain anticancer properties. The specific mechanism of the anticancer activity is unknown. Methods: To study the anticancer mechanism of carrimycin, we synthesized [...] Read more.
Background: Carrimycin is a mixture of spiramycin derivatives with antibacterial functions. However, recent studies have shown that it possesses certain anticancer properties. The specific mechanism of the anticancer activity is unknown. Methods: To study the anticancer mechanism of carrimycin, we synthesized a derivative of spiramycin, n-hexyl spiramycin (h-SPM), and used a combination of metabolomics and transcriptomics methods. Capillary electrophoresis–mass spectrometry (CE-MS) was used to detect polar small molecule metabolites, and liquid chromatography–mass spectrometry (LC-MS) was used to detect lipid metabolites in cells. Transcriptomics was used to measure mRNA content in cells. Finally, by processing these data using specific bioinformatics methods, the mechanism underlying anticancer effect of carrimycin was determined. Results: Metabolomics and transcriptomic results showed that lipid metabolism and mitochondrial biogenesis pathways in the cells changed after hSPM treatment, NR1D1 genes and ceramide were enriched from these pathways, implicating the involvement of ROS and pro-inflammatory response. Western blotting verified that the protein levels of NR1D1 decreased after h-SPM treatment, and ROS stating and qPCR demonstrated that ROS levels and the mRNA levels of pro-inflammatory genes were greatly induced by h-SPM. Conclusions: h-SPM reduced the protein level of NR1D1, disrupted metabolic regulation, accumulating ceramide, and the subsequent increased ROS generation promoted apoptosis and pro-inflammatory-like response of cells. Our findings unveiled the anticancer mechanism of a potent anticancer derivative of spiramycin and unveiled its mechanism of action. Full article
(This article belongs to the Special Issue Cell Death and Cancer Metabolism)
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15 pages, 3827 KB  
Article
Antagonizing the S1P-S1P3 Axis as a Promising Anti-Angiogenic Strategy
by Sofia Avnet, Emi Mizushima, Beatrice Severino, Maria Veronica Lipreri, Antonia Scognamiglio, Angela Corvino, Nicola Baldini and Margherita Cortini
Metabolites 2025, 15(3), 178; https://doi.org/10.3390/metabo15030178 - 5 Mar 2025
Cited by 1 | Viewed by 1139
Abstract
Background: Angiogenesis, the process of new blood vessel formation, is critically regulated by a balance of pro- and anti-angiogenic factors. This process plays a central role in tumor progression and is modulated by tumor cells. Sphingosine-1-phosphate (S1P), a bioactive lipid signaling molecule acting [...] Read more.
Background: Angiogenesis, the process of new blood vessel formation, is critically regulated by a balance of pro- and anti-angiogenic factors. This process plays a central role in tumor progression and is modulated by tumor cells. Sphingosine-1-phosphate (S1P), a bioactive lipid signaling molecule acting via G-protein-coupled receptors (S1PR1–5), has emerged as a key mediator of vascular development and pathological angiogenesis in cancer. Consequently, targeting the S1P-S1PRs axis represents a promising strategy for antiangiogenic therapies. This study explores S1PR3 as a potential therapeutic target in osteosarcoma, the most common primary bone malignancy, which we have previously demonstrated to secrete S1P within the acidic tumor microenvironment. Methods: The effects of KRX-725-II and its derivatives, Tic-4-KRX-725-II and [D-Tic]4-KRX-725-II—pepducins acting as S1PR3 antagonists as allosteric modulators of GPCR activity—were tested on metastatic osteosarcoma cells (143B) for proliferation and migration inhibition. Anti-angiogenic activity was assessed using endothelial cells (HUVEC) through proliferation and tubulogenesis assays in 2D, alongside sprouting and migration analyses in a 3D passively perfused microfluidic chip. Results: S1PR3 inhibition did not alter osteosarcoma cell growth or migration. However, it impaired endothelial cell tubulogenesis up to 75% and sprouting up to 30% in respect to controls. Conventional 2D assays revealed reduced tubule nodes and length, while 3D microfluidic models demonstrated diminished sprouting area and maximum migration distance, indicating S1PR3’s role in driving endothelial cell differentiation. Conclusions: These findings highlight S1PR3 as a critical regulator of angiogenesis and posit its targeting as a novel anti-angiogenic strategy, particularly for aggressive, S1P-secreting tumors with pronounced metastatic potential and an acidic microenvironment. Full article
(This article belongs to the Special Issue Cell Death and Cancer Metabolism)
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