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Molecular Advances in Cancer and Cell Metabolism
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Molecular Advances in Cancer and Cell Metabolism

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

Deadline for manuscript submissions: 31 August 2024 | Viewed by 2480

Special Issue Editors

Dr. Maria Concetta Faniello

E-Mail Website
Guest Editor
Research Center of Biochemistry and Advanced Molecular Biology, Department of Experimental and Clinical Medicine, “Magna Graecia” University of Catanzaro, 88100 Catanzaro, Italy
Interests: cell metabolism; antioxidants; transcription factors; gene expression; cancer metabolism
Dr. Maria Mesuraca

E-Mail Website
Guest Editor
Department of Experimental and Clinical Medicine, University Magna Græcia, 88100 Catanzaro, Italy
Interests: cell metabolism; gene transfer; cell differentiation; signaling pathways; transcription factors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Over the years, studies of cellular functions have allowed us to highlight how metabolism can be reprogrammed to support its links to many biological processes ranging from macromolecular synthesis to ATP production; in addition, cells continuously respond to different stimuli, growth factors, hormones, and changes in nutrient uptake by adapting metabolism to new conditions. Accumulating evidence suggests that metabolism can also regulate gene expression and signaling pathways, and its changes have significant impacts on many human diseases as well as recognized conditions associated with cancer.

The cellular metabolic phenotype is determined by the availability of metabolic substrates, oxygen levels, and interactions with the microenvironment where cells can proliferate and differentiate. The reprogramming of energy metabolism is a recognized hallmark of cancer cells that allows adaptation to new conditions of cell growth/survival through the metabolic switch from oxidative phosphorylation to glycolysis, when the aberrant proliferative capacity of cancer cells increases the energetic demands contributing to the neoplastic transformation.

The aim of this Special Issue is to collect the current advances of the metabolic regulation in human normal and tumor cells to better characterize the biochemical mechanism differences associated with tumor metabolic reprogramming. Original articles, short communications, and reviews from physiological and pathological molecular pathways such as those regarding integrative omics techniques are welcome.

We look forward to receiving your contributions.

Dr. Maria Concetta Faniello
Dr. Maria Mesuraca
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

  • cell metabolism
  • cancer metabolism
  • cancer cell
  • oxidative stress
  • gene expression
  • signaling pathways
  • metabolic regulation
  • tumor growth
  • energy metabolism
  • metabolic phenotype
  • metabolic substrates

Published Papers (3 papers)

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Research

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15 pages, 2331 KiB  
Article
Synergy between PEDF and Doxorubicin in Breast Cancer Cells: Effects on Metastatic and Metabolic Pathways
by Raziyeh Abooshahab, Hani Al-Salami and Crispin R. Dass
Int. J. Mol. Sci. 2024, 25(5), 2755; https://doi.org/10.3390/ijms25052755 - 27 Feb 2024
Viewed by 790
Abstract
Pigment epithelium-derived factor (PEDF), a serine protease inhibitor (Serpin) family member, shows promise in inhibiting tumour growth. In our study, we explored the effects of PEDF on the efficacy of the frontline chemotherapy agent doxorubicin (Dox) in BC cells. We found that Dox+PEDF [...] Read more.
Pigment epithelium-derived factor (PEDF), a serine protease inhibitor (Serpin) family member, shows promise in inhibiting tumour growth. In our study, we explored the effects of PEDF on the efficacy of the frontline chemotherapy agent doxorubicin (Dox) in BC cells. We found that Dox+PEDF treatment significantly reduced glucose uptake in MDA-MB-231 cells compared to the control (p = 0.0005), PEDF (p = 0.0137), and Dox (p = 0.0171) alone but paradoxically increased it in MCF-7 cells. Our findings further revealed that PEDF, Dox, and Dox+PEDF substantially hindered tumour cell migration from tumour spheroids, with Dox+PEDF showing the most significant impact (p < 0.0001). We also observed notable decreases in the expression of metastatic markers (uPAR, uPA, CXCR4, MT1-MMP, TNF-α) across all treatment groups (p < 0.0001) in both cell lines. When it comes to metabolic pathways, PEDF increased phosphorylated IRS-1 (p-IRS1) levels in MDA-MB-231 and MCF-7 (p < 0.0001), while Dox decreased it, and the combination led to an increase. In MDA-MB-231 cells, treatment with PEDF, Dox, and the combination led to a notable decrease in both phosphorylated AKT (p-AKT) and total AKT levels. In MCF-7, while PEDF, Dox, and their combination led to a reduction in p-AKT, total levels of AKT increased in the presence of Dox and Dox+PEDF. Combining PEDF with Dox enhances the targeting of metastatic and metabolic pathways in breast cancer cell lines. This synergy, marked by PEDF’s increasing roles in cancer control, may pave the way for more effective cancer treatments. Full article
(This article belongs to the Special Issue Molecular Advances in Cancer and Cell Metabolism)
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Review

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20 pages, 1412 KiB  
Review
Exploring the Enigma: The Role of the Epithelial Protein Lost in Neoplasm in Normal Physiology and Cancer Pathogenesis
by Emma Lindell and Xiaonan Zhang
Int. J. Mol. Sci. 2024, 25(9), 4970; https://doi.org/10.3390/ijms25094970 - 02 May 2024
Viewed by 197
Abstract
The cytoskeleton plays a pivotal role in maintaining the epithelial phenotype and is vital to several hallmark processes of cancer. Over the past decades, researchers have identified the epithelial protein lost in neoplasm (EPLIN, also known as LIMA1) as a key regulator of [...] Read more.
The cytoskeleton plays a pivotal role in maintaining the epithelial phenotype and is vital to several hallmark processes of cancer. Over the past decades, researchers have identified the epithelial protein lost in neoplasm (EPLIN, also known as LIMA1) as a key regulator of cytoskeletal dynamics, cytoskeletal organization, motility, as well as cell growth and metabolism. Dysregulation of EPLIN is implicated in various aspects of cancer progression, such as tumor growth, invasion, metastasis, and therapeutic resistance. Its altered expression levels or activity can disrupt cytoskeletal dynamics, leading to aberrant cell motility and invasiveness characteristic of malignant cells. Moreover, the involvement of EPLIN in cell growth and metabolism underscores its significance in orchestrating key processes essential for cancer cell survival and proliferation. This review provides a comprehensive exploration of the intricate roles of EPLIN across diverse cellular processes in both normal physiology and cancer pathogenesis. Additionally, this review discusses the possibility of EPLIN as a potential target for anticancer therapy in future studies. Full article
(This article belongs to the Special Issue Molecular Advances in Cancer and Cell Metabolism)
18 pages, 1941 KiB  
Review
A Systematic Review of the Metabolism of High-Grade Gliomas: Current Targeted Therapies and Future Perspectives
by Lucio De Maria, Pier Paolo Panciani, Marco Zeppieri, Tamara Ius, Simona Serioli, Amedeo Piazza, Emanuele Di Giovanni, Marco Maria Fontanella and Edoardo Agosti
Int. J. Mol. Sci. 2024, 25(2), 724; https://doi.org/10.3390/ijms25020724 - 05 Jan 2024
Viewed by 929
Abstract
High-grade glial tumors (HGGs) exhibit aggressive growth patterns and high recurrence rates. The prevailing treatment approach comprises radiation therapy (RT), chemotherapy (CMT), and surgical resection. Despite the progress made in traditional treatments, the outlook for patients with HGGs remains bleak. Tumor metabolism is [...] Read more.
High-grade glial tumors (HGGs) exhibit aggressive growth patterns and high recurrence rates. The prevailing treatment approach comprises radiation therapy (RT), chemotherapy (CMT), and surgical resection. Despite the progress made in traditional treatments, the outlook for patients with HGGs remains bleak. Tumor metabolism is emerging as a potential target for glioma therapies, a promising approach that harnesses the metabolism to target tumor cells. However, the efficacy of therapies targeting the metabolism of HGGs remains unclear, compelling a comprehensive review. This study aimed to assess the outcome of present trials on HGG therapies targeting metabolism. A comprehensive search of PubMed, Ovid MEDLINE, and Ovid EMBASE was conducted until November 2023. The search method used pertinent Medical Subject Heading (MeSH) terminologies and keywords referring to “high-grade gliomas”, “metabolism”, “target therapies”, “monoclonal antibodies”, “overall survival”, and “progression-free survival”. The review analyzed studies that focused on therapies targeting the metabolism of HGGs in human subjects. These studies included both randomized controlled trials (RCTs) and non-randomized controlled trials (NRCTs). Out of 284 articles identified, 23 trials met the inclusion criteria and were thoroughly analyzed. Phase II trials were the most numerous (62%). Targeted metabolic therapies were predominantly used for recurrent HGGs (67%). The most common targeted pathways were the vascular endothelial growth factor (VEGF, 43%), the human epidermal growth factor receptor (HER, 22%), the platelet-derived growth factor (PDGF, 17%), and the mammalian target of rapamycin (mTOR, 17%). In 39% of studies, the subject treatment was combined with CMT (22%), RT (4%), or both (13%). The median OS widely ranged from 4 to 26.3 months, while the median PFS ranged from 1.5 to 13 months. This systematic literature review offers a thorough exploration of the present state of metabolic therapies for HGGs. The multitude of targeted pathways underscores the intricate nature of addressing the metabolic aspects of these tumors. Despite existing challenges, these findings provide valuable insights, guiding future research endeavors. The results serve as a foundation for refining treatment strategies and enhancing patient outcomes within the complex landscape of HGGs. Full article
(This article belongs to the Special Issue Molecular Advances in Cancer and Cell Metabolism)
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