Inorganic arsenic (iAs) is an environmental toxicant currently poisoning millions of people worldwide, and chronically exposed individuals are susceptible to arsenicosis or arsenic poisoning. Using a state-of-the-art technique to map the methylomes of our study subjects, we identified a large interactome of hypermethylated genes that are enriched for their involvement in arsenic-associated diseases, such as cancer, heart disease, and diabetes. Notably, we have uncovered an arsenic-induced tumor suppressorome, a complex of 17 tumor suppressors known to be silenced in human cancers. This finding represents a pivotal clue in unraveling a possible epigenetic mode of arsenic-induced disease.
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http://dx.doi.org/10.1021/tx1004419 | DOI Listing |
J Invest Dermatol
January 2025
Department of Dermatology, Xiangya Hospital, Central South University, Changsha, China; National Engineering Research Center of Personalized Diagnostic and Therapeutic Technology, Changsha, China; Furong Laboratory, Changsha, China; Hunan Key Laboratory of Skin Cancer and Psoriasis, Hunan Engineering Research Center of Skin Health and Disease, Xiangya Hospital, Central South University, Changsha, China; National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Changsha, China. Electronic address:
Melanoma is a devastating form of skin cancer characterized by a high mutational burden, limited treatment success, and dismal prognosis. Although immunotherapy and targeted therapies have significantly revolutionized melanoma treatment, the majority of patients fail to achieve durable responses, highlighting the urgent need for novel therapeutic strategies. Ferroptosis, an iron-dependent form of regulated cell death driven by the overwhelming accumulation of lipid peroxides, has emerged as a promising therapeutic approach in preclinical melanoma models.
View Article and Find Full Text PDFJ Clin Med
December 2024
Molecular Biology Department, Surgery and Cardiovascular Biomedicine, National Institute of Cardiology Ignacio Chávez, Juan Badiano 1, Tlalpan, Mexico City 14080, Mexico.
Aortic valve calcification results from degenerative processes associated with several pathologies. These processes are influenced by age, chronic inflammation, and high concentrations of phosphate ions in the plasma, which contribute to induce mineralization in the aortic valve and deterioration of cardiovascular health. Environmental factors, such as wood smoke that emits harmful and carcinogenic pollutants, carbon monoxide (CO), and nitrogen oxide (NO), as well as other reactive compounds may also be implicated.
View Article and Find Full Text PDFCancers (Basel)
December 2024
Hugo W. Moser Research Institute at Kennedy Krieger, Baltimore, MD 21205, USA.
: CSCs are critical drivers of the tumor and stem cell phenotypes of glioblastoma (GBM) cells. Chromatin modifications play a fundamental role in driving a GBM CSC phenotype. The goal of this study is to further our understanding of how stem cell-driving events control changes in chromatin architecture that contribute to the tumor-propagating phenotype of GBM.
View Article and Find Full Text PDFNutrients
December 2024
Department of Nutrition, Texas A&M University, College Station, TX 77843, USA.
Background/objectives: This study builds on previous findings from mouse models, which showed that maternal overnutrition induced by a high-fat diet (HFD) promotes metabolic-associated fatty liver disease (MAFLD) in offspring, linked to global DNA hypermethylation. We explored whether epigenetic modulation with 5-Aza-CdR, a DNA methylation inhibitor, could prevent MAFLD in offspring exposed to maternal overnutrition.
Methods: The offspring mice from dams of maternal overnutrition were fed either a chow diet or a high-fat diet (HFD) for 10 weeks.
Int J Mol Sci
January 2025
Departamento de Biología Molecular y Bioquímica, Universidad de Málaga, 29071 Málaga, Spain.
Glutaminase controls the first step in glutaminolysis, impacting bioenergetics, biosynthesis and oxidative stress. Two isoenzymes exist in humans, GLS and GLS2. GLS is considered prooncogenic and overexpressed in many tumours, while GLS2 may act as prooncogenic or as a tumour suppressor.
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