Cancer cell metabolism differs significantly from the metabolism of non-transformed cells. This altered metabolic reprogramming mediates changes in the uptake and use of nutrients that permit high rates of proliferation, growth, and survival. The androgen receptor (AR) plays an essential role in the establishment and progression of prostate cancer (PCa), and in the metabolic adaptation that takes place during this progression. In its role as a transcription factor, the AR directly affects the expression of several effectors and regulators of essential catabolic and biosynthetic pathways. Indirectly, as a modulator of the one-carbon metabolism, the AR can affect epigenetic processes, DNA metabolism, and redox balance, all of which are important factors in tumorigenesis. In this review, we focus on the role of AR-signaling on one-carbon metabolism in tumorigenesis. Clinical implications of one-carbon metabolism and AR-targeted therapies for PCa are discussed in this context.
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http://dx.doi.org/10.3390/ijms17081208 | DOI Listing |
Expert Rev Proteomics
January 2025
Research Unit for Molecular Medicine, Department of Clinical Medicine, Faculty of Health, Aarhus University, Denmark.
Introduction: Mitochondria contain multiple pathways including energy metabolism and several signaling and synthetic pathways. Mitochondrial proteomics is highly valuable for studying diseases including inherited metabolic disorders, complex and common disorders like neurodegeneration, diabetes and cancer, since they all to some degree have mitochondrial underpinnings.
Areas Covered: The main mitochondrial functions and pathways are outlined and systematic protein lists are presented.
Cancer Res
January 2025
First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Sunitinib is a first-line targeted therapy for patients with renal cell carcinoma (RCC), but resistance represents a significant obstacle to the treatment of advanced and metastatic RCC. Metabolic reprogramming is a characteristic of RCC, and changes in metabolic processes might contribute to resistance to sunitinib. Here, we identified MTHFD2, a mitochondrial enzyme involved in one-carbon metabolism, as a critical mediator of sunitinib resistance in RCC.
View Article and Find Full Text PDFMol Genet Metab Rep
March 2025
The Shmunis School of Biomedicine and Cancer Research, The George S. Wise Faculty for Life Sciences, Sagol School of Neurosciences, Tel Aviv University, 6997801 Tel Aviv, Israel.
Dihydrolipoamide dehydrogenase (DLD) deficiency is an autosomal recessive disorder characterized by a functional disruption in several critical mitochondrial enzyme complexes, including pyruvate dehydrogenase and α-ketoglutarate dehydrogenase. Despite DLD's pivotal role in cellular energy metabolism, detailed molecular and metabolic consequences of DLD deficiency (DLDD) remain poorly understood. This study represents the first in-depth multi-omics analysis, specifically metabolomic and transcriptomic, of fibroblasts derived from a DLD-deficient patient compound heterozygous for a common Ashkenazi Jewish variant (c.
View Article and Find Full Text PDFFood Chem
January 2025
Department of Food Science and Technology, Jinan University, Guangzhou 510632, China. Electronic address:
As an essential B vitamin, folate participates in one‑carbon metabolism. The 5-methyltetrahydrofolate (5-MTHF) avoids the drawbacks associated with folic acid and native folylpolyglutamate folate in food, thereby emerging as a superior alternative to folate supplement. To enhance the stability and digestibility of 5-MTHF, nanoliposome (NL) was modified using a layer-by-layer self-assembly method with chitosan (CH) and pectin (P).
View Article and Find Full Text PDFNutrients
December 2024
Departments of Human Genetics and Pediatrics, McGill University, Montreal, QC H3A 0C7, Canada.
Background/objectives: The gene variant results in a thermolabile MTHFR enzyme associated with elevated plasma homocysteine in TT individuals. Health risks associated with the TT genotype may be modified by dietary and supplemental folate intake. Supplementation with methyltetrahydrofolate (methylTHF) may be preferable to folic acid because it is the MTHFR product, and does not require reduction by DHFR to enter one-carbon folate metabolism.
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