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TET1:The epigenetic architect of clinical disease progression
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作者 keyvan jabbari Ali Khalafizadeh +2 位作者 Mahboubeh Sheikhbahaei Hossein Soltaninejad Sadegh Babashah 《Genes & Diseases》 2025年第5期129-149,共21页
The ten-eleven translocation 1(TET1)protein,a member of the humanα-ketoglutarate-dependent dioxygenase TET family,functions as a 5-methylcytosine hydroxylase with a strong affinity for genomic regions enriched with 5... The ten-eleven translocation 1(TET1)protein,a member of the humanα-ketoglutarate-dependent dioxygenase TET family,functions as a 5-methylcytosine hydroxylase with a strong affinity for genomic regions enriched with 5′-CpG-3′dinucleotides,particularly CpG islands.TET1 is critical in initiating DNA demethylation and maintaining a balanced interaction between demethylation and DNA methylation,which is essential for genomic methylation stability and precise epigenetic regulation.By removing methyl groups from specific tumor suppressor genes,TET1 can influence their expression.This review summarizes the latest advancements in TET1 research,emphasizing its role in demethylation mechanisms and its significance in regulatory processes related to clinical conditions.TET1 is a crucial mediator of demethylation,although the precise details of this mechanism are not yet fully understood.Additionally,TET1 plays a key role in inhibiting tumor progression,but its effects vary across different tumors.This variability arises from its interactions with diverse signaling pathways,where it can function either as an antagonist or a promoter.The role of TET1 remains controversial in certain cancer types,and its potential oncogenic functions have attracted growing interest,opening new avenues for investigation. 展开更多
关键词 Clinical diseases DNA demethylation EPIGENETICS TET1 Therapeutic target
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