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Molecular Advances in Cancer and Cell Metabolism—2nd Edition
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Molecular Advances in Cancer and Cell Metabolism—2nd Edition

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: 30 June 2025 | Viewed by 1018

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: iron-regulatory proteins; apoferritins; gene; cell death; phospholipid-hydroperoxide glutathione peroxidase; antiporters
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Mesuraca

E-Mail Website
Guest Editor
Department of Experimental and Clinical Medicine, University Magna Græcia, 88100 Catanzaro, Italy
Interests: haematopoietic stem cells; biochemistry metabolism; gene transfer; osteoblastogenesis; transcription factors
Special Issues, Collections and Topics in MDPI journals
Dr. Barbara Quaresima

E-Mail Website
Guest Editor
Department of Experimental and Clinical Medicine, University Magna Græcia, 88100 Catanzaro, Italy
Interests: cancer metabolism; gene expression; molecular pathways; omics analysis

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 on physiological and pathological molecular pathways, including those that focus integrative omics techniques, are welcome.

We look forward to receiving your contributions.

Dr. Maria Concetta Faniello
Dr. Maria Mesuraca
Dr. Barbara Quaresima
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

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Published Papers (2 papers)

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Research

20 pages, 7746 KiB  
Article
PBX3-HMGCR Axis Promotes Hepatocellular Carcinoma Progression Through Enhancing De Novo Cholesterol Biosynthesis
by Xia Zhang, Li Qiu, Lei Zhang, Wenfang Li, Debing Xiang, Jian Wang, Shourong Wu and Vivi Kasim
Int. J. Mol. Sci. 2025, 26(11), 5210; https://doi.org/10.3390/ijms26115210 - 29 May 2025
Viewed by 249
Abstract
Tumor cells alter lipid metabolic pathways to meet their demands for energy and membrane biosynthesis. Despite its crucial role in tumor cell growth, survival, and metastasis, the mechanisms underlying tumor cell lipid metabolic reprogramming remain poorly understood. Pre-B-cell leukemia transcription factor 3 (PBX3), [...] Read more.
Tumor cells alter lipid metabolic pathways to meet their demands for energy and membrane biosynthesis. Despite its crucial role in tumor cell growth, survival, and metastasis, the mechanisms underlying tumor cell lipid metabolic reprogramming remain poorly understood. Pre-B-cell leukemia transcription factor 3 (PBX3), a member of the PBX family, could promote tumorigenesis; however, whether it is involved in tumor lipid metabolic reprogramming remains unknown. Herein, we found that PBX3 significantly promotes tumor growth by enhancing lipid accumulation in HCC cells. By assessing the effect of PBX3 on the expression levels of lipid metabolism-related genes, we found that PBX3 could positively regulate the expression of 3-hydroxy-3-methylglutaryl CoA reductase (HMGCR), a rate-limiting enzyme in the cholesterol biosynthesis pathway. Mechanistically, we revealed that PBX3 could directly bind to the −167/−151 region of HMGCR promoter, thereby increasing its transcriptional activity and, subsequently, its expression level. This leads to the increase of HCC cell cholesterol biosynthesis and, eventually, to the increase of the in vivo tumorigenic potential. Collectively, our research revealed an unprecedented regulatory mechanism of cholesterol metabolism in HCC cells through PBX3 positive regulation on HMGCR expression levels. These findings provide novel insights into tumor metabolic reprogramming and uncover a previously unknown physiological function for PBX3. Moreover, these results suggest the potential of targeting PBX3 as an anti-tumor therapeutic strategy. Full article
(This article belongs to the Special Issue Molecular Advances in Cancer and Cell Metabolism—2nd Edition)
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16 pages, 1024 KiB  
Article
PI3K and PINK1 Immunoexpression as Predictors of Survival in Patients Undergoing Resection of Brain Metastases from Lung Adenocarcinoma
by Miriam Rubiera-Valdés, Mª Daniela Corte-Torres, Andrea Navarro-López, Noelia Blanco-Agudín, Santiago Fernández-Menéndez, Kelvin M. Piña-Batista, Jorge Santos-Juanes, Jesús Merayo-Lloves, Luis M. Quirós, Adela A. Fernández-Velasco and Iván Fernández-Vega
Int. J. Mol. Sci. 2025, 26(7), 2945; https://doi.org/10.3390/ijms26072945 - 24 Mar 2025
Viewed by 455
Abstract
Phosphoinositide 3-kinase (PI3K) and PTEN-induced kinase 1 (PINK1) are key regulators of metabolism and mitochondrial quality control. This study assessed their immunoexpression in 22 patients with lung adenocarcinoma and resected brain metastases who underwent curative treatment between 2007 and 2017 and evaluated their [...] Read more.
Phosphoinositide 3-kinase (PI3K) and PTEN-induced kinase 1 (PINK1) are key regulators of metabolism and mitochondrial quality control. This study assessed their immunoexpression in 22 patients with lung adenocarcinoma and resected brain metastases who underwent curative treatment between 2007 and 2017 and evaluated their prognostic significance. Tissue microarrays of primary tumors and matched metastases were analyzed using the H-score method. PI3K expression was significantly higher in primary tumors (96.8 ± 57.9 vs. 43.5 ± 62.3; p = 0.003) and in stage IV adenocarcinomas (113.3 ± 56.3 vs. 61.4 ± 47.1; p = 0.043). PINK1 expression showed no significant variation across disease stages. Univariate analysis identified older age (>55 years), PI3K overexpression (HR = 7.791, 95% CI 1.718–36.432; >50 points), and PINK1 overexpression (>100 points) in primary tumors as predictors of poor overall survival (HR = 2.236, 95% CI 1.109–4.508; p = 0.025). Multivariate analysis confirmed PINK1 overexpression in primary tumors as an independent prognostic factor (HR = 4.328, 95% CI 1.264–14.814; p = 0.020). These findings suggest that PI3K and PINK1 may serve as prognostic biomarkers in lung adenocarcinoma with resected brain metastases, emphasizing the need for research on their role in tumor progression and therapeutic response. Full article
(This article belongs to the Special Issue Molecular Advances in Cancer and Cell Metabolism—2nd Edition)
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