image: TET1-mediated transcriptional activation through promoter demethylation. This figure illustrates the mechanism by which TET1 facilitates gene transcription through the demethylation of promoter regions. The schematic diagram demonstrates TET1's enzymatic activity, which catalyzes DNA demethylation, ultimately leading to the activation of gene expression. Image link: https://ars.els-cdn.com/content/image/1-s2.0-S2352304225000029-gr1_lrg.jpg
Credit: Genes & Diseases
Recent findings shed new light on the critical role of TET1, a pivotal player in epigenetic regulation, in the development and progression of various clinical diseases. As an enzyme responsible for DNA demethylation, TET1 influences gene expression by modifying methylcytosine levels, which are crucial for maintaining genomic stability and proper cellular function.
A deeper understanding of TET1’s function has unveiled its dual role in disease progression. In certain cancers, TET1 acts as a tumor suppressor, inhibiting malignant cell growth by preventing the hypermethylation of crucial regulatory genes. Conversely, in other cancer types, TET1 upregulation has been linked to tumor progression, driving oncogenic pathways that enhance cell proliferation, invasion, and survival. The complexity of TET1’s behavior highlights its interaction with multiple signaling pathways, making it both a target for therapeutic intervention and a marker for disease prognosis.
Beyond cancer, TET1 plays an integral role in neurological disorders, metabolic diseases, and autoimmune conditions. In the brain, TET1 contributes to neural plasticity and cognitive function, with dysregulation implicated in disorders such as schizophrenia, Alzheimer’s disease, and bipolar disorder. Studies suggest that abnormal TET1 activity can disrupt critical epigenetic mechanisms, affecting gene expression patterns related to neurodevelopment and synaptic function.
In the realm of metabolic diseases, TET1 has been found to regulate fat metabolism and glucose homeostasis, influencing the onset of conditions such as obesity and diabetes. By controlling the expression of metabolic regulators, TET1 appears to be a crucial player in maintaining energy balance and preventing metabolic dysfunction. Furthermore, its role in inflammatory diseases and immune system regulation underscores its potential impact on disorders like rheumatoid arthritis and systemic sclerosis, where abnormal epigenetic modifications contribute to immune dysregulation.
Given its broad influence across various diseases, TET1 is emerging as a compelling target for novel therapeutic strategies. Scientists are actively exploring TET1 inhibitors and activators to manipulate its epigenetic functions for potential clinical applications. While challenges remain in developing targeted therapies, advancements in epigenetic research are paving the way for precision medicine approaches that harness TET1’s unique regulatory capabilities.
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Reference
Keyvan Jabbari, Ali Khalafizadeh, Mahboubeh Sheikhbahaei, Hossein Soltaninejad, Sadegh Babashah, TET1: The epigenetic architect of clinical disease progression, Genes & Diseases, Volume 12, Issue 5, 2025, 101513, https://doi.org/10.1016/j.gendis.2025.101513
Journal
Genes & Diseases