With the growing advent of nanotechnology in medicine (therapeutic, diagnostic and imaging applications), cosmetics, electronics, clothing and food industries, exposure to nanomaterials (NMs) is on the rise and therefore exploring their toxic biological effects have gained great significance. In vitro and in vivo studies over the last decade have revealed that NMs have the potential to cause cytotoxicity and genotoxicity although some contradictory reports exist. However, there are only few studies which have explored the epigenetic mechanisms (changes to DNA methylation, histone modification and miRNA expression) of NM-induced toxicity, and there is a scarcity of information and many questions in this area remain unexplored and unaddressed. This review comprehensively describes the epigenetic mechanisms involved in the induction of toxicity of engineered NMs, and provides comparisons between similar effects observed upon exposure to small or nanometer-sized particles. Lastly, gaps in existing literature and scope for future studies that improve our understanding of NM-induced epigenetic toxicity are discussed.
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http://dx.doi.org/10.2217/epi.15.3 | DOI Listing |
J Clin Invest
January 2025
Department of Biochemistry and Molecular Genetics and.
Mutations or homozygous deletions of MHC class II (MHC-II) genes are commonly found in B cell lymphomas that develop in immune-privileged sites and have been associated with patient survival. However, the mechanisms regulating MHC-II expression, particularly through genetic and epigenetic factors, are not yet fully understood. In this study, we identified a key signaling pathway involving the histone H2AK119 deubiquitinase BRCA1 associated protein 1 (BAP1), the interferon regulatory factor interferon regulatory factor 1 (IRF1), and the MHC-II transactivator class II transactivator (CIITA), which directly activates MHC-II gene expression.
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Department of Biochemistry, Faculty of Sciences, King Abdulaziz University, Jeddah, 21589, Saudi Arabia.
Cancer is one of the most devastating illnesses in the world, impacting millions of individuals every year. Despite various therapies, the final effect is unsatisfactory. Chemotherapy currently dominates as the primary option of treatment.
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January 2025
Division of Cancer Biology, Laboratory Animal Center, Fourth Military Medical University, Xi'an, Shaanxi 710032, China.
Bone metastasis and skeletal-related complications are primary causes of mortality in advanced-stage prostate cancer (PCa). Epigenetic regulation, particularly histone modification, plays a key role in this process; however, the underlying mechanisms remain elusive. In mouse models, JARID1D was an important mediator of both visceral and bone metastases.
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January 2025
Department of Integrative Oncology, Fudan University Shanghai Cancer Center, and Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China.
Circular RNA (circRNA) has gained attention as a promising platform for mRNA vaccines due to its stability, sustained protein expression, and intrinsic immunostimulatory properties. This study aimed to design and optimize a circRNA cancer vaccine platform by screening for efficient internal ribosome entry sites (IRES) and enhancing circRNA translation efficiency for improved cancer immunotherapy. We screened 29 IRES elements to identify the most efficient one for immune cell translation, ultimately discovering the A (EV-A) IRES.
View Article and Find Full Text PDFAntioxid Redox Signal
January 2025
Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Growing evidence indicates the importance of redox reactions homeostasis, mediated predominantly by reactive oxygen species (ROS) in influencing the development, differentiation, progression, metastasis, programmed cell death, tumor microenvironment, and therapeutic resistance of cancer. Therefore, reviewing the ROS-linked epigenetic changes in cancer is fundamental to understanding the progression and prevention of cancer. We review in depth the molecular mechanisms involved in ROS-mediated epigenetic changes that lead to alteration of gene expression by altering DNA, modifying histones, and remodeling chromatin and noncoding RNA.
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