A large number of studies have revealed that epigenetics plays an important role in cancer development. However, the currently-developed epigenetic drugs cannot achieve a stable curative effect. Thus, it may be necessary to redefine the role of epigenetics in cancer development. It has been shown that embryonic development and tumor development share significant similarities in terms of biological behavior and molecular expression patterns, and epigenetics may be the link between them. Cell differentiation is likely a manifestation of epigenetic homeostasis at the cellular level. In this article, we introduced the importance of epigenetic homeostasis in cancer development and analyzed the shortcomings of current epigenetic treatment regimens. Understanding the dynamic process of epigenetic homeostasis in organ development can help us characterize cancer according to its differentiation stages, explore new targets for cancer treatment, and improve the clinical prognosis of patients with cancer.
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http://dx.doi.org/10.3389/fonc.2021.747022 | DOI Listing |
Oxid Med Cell Longev
December 2024
Center for Global Health, Università Cattolica del Sacro Cuore (UCSC), Rome, Italy.
Vitiligo is a skin disease that affects all ethnicities and genders and is characterized by the loss of pigment essentially due to the selective loss of melanocytes. Although it is generally considered a systemic disease associated with polymorphisms in genes involved in the immune response, vitiligo is also considered an oxidative imbalance-associated disease. It represents a multifactorial pathology in which some genetic predisposition and epigenetic factors coupled with some critical biochemical and molecular pathways could play a pivotal role.
View Article and Find Full Text PDFBone
December 2024
Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine, Zhejiang Provincial Clinical Research Centre for Oral Diseases, Key Laboratory of Oral Biomedical Research of Zhejiang Province, Cancer Centre of Zhejiang University, Engineering Research Center of Oral Biomaterials and Devices of Zhejiang Province, Hangzhou 310000, China. Electronic address:
Metabolic pathways exhibit fluctuating activities during bone and dental loss and defects, suggesting a regulated metabolic plasticity. Skeletal remodeling is an energy-demanding process related to altered metabolic activities. These metabolic changes are frequently associated with epigenetic modifications, including variations in the expression or activity of enzymes modified through epigenetic mechanisms, which directly or indirectly impact cellular metabolism.
View Article and Find Full Text PDFCancer Lett
December 2024
Department of Anatomy and Cell Biology, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA; The George Washington University Cancer Center, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA. Electronic address:
Cellular plasticity in prostate cancer promotes treatment resistance. Several independent studies have used mouse models, single-cell RNA sequencing, and genetic lineage tracing approaches to characterize cellular differentiation and plasticity during prostate organogenesis, homeostasis and androgen-mediated tissue regeneration. We review these findings and recent work using immune-competent genetically-engineered mouse models to characterize cellular plasticity and clonal dynamic changes during prostate cancer progression.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Department of Medical Biochemistry, School of Medicine, Koc University, Istanbul, Türkiye.
Aging is influenced by cellular senescence mechanisms that are associated with oxidative stress. Oxidative stress is the imbalance between antioxidants and free radicals. This imbalance affects enzyme activities and causes mitochondrial dysfunction.
View Article and Find Full Text PDFSheng Wu Gong Cheng Xue Bao
December 2024
College of Veterinary Medicine, Southwest University, Chongqing 402460, China.
Ten-eleven translocation 1 (TET1) protein is an alpha-ketoglutaric acid (α-KG) and Fe-dependent dioxygenase. It plays a role in the active demethylation of DNA by hydroxylation of 5-methyl-cytosine (5-mC) to 5-hydroxymethyl-cytosine (5-hmC). Ten-eleven translocation 1 (TET1) protein is involved in maintaining genome methylation homeostasis and epigenetic regulation.
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