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A Review of Research on the Mechanism of Tumor Regulation by N-Acetyltransferase 10.
Cai, Teng; Lin, Yanyan; Meng, Wenbo.
Afiliação
  • Cai T; The First Clinical Medical College, Lanzhou University, 730000 Lanzhou, Gansu, China.
  • Lin Y; The Department of General Surgery, The First Hospital of Lanzhou University, 730000 Lanzhou, Gansu, China.
  • Meng W; The Department of General Surgery, The First Hospital of Lanzhou University, 730000 Lanzhou, Gansu, China.
Discov Med ; 36(186): 1334-1344, 2024 Jul.
Article em En | MEDLINE | ID: mdl-39054704
ABSTRACT
N-acetyltransferase 10 (NAT10) is an important acetyltransferase that regulates telomerase activity and participates in DNA damage reactions, ribosomal RNA (rRNA) transcriptional activation, cell division, microtubule acetylation, and other important cellular processes. Abnormalities in the expression or distribution of NAT10 result in diseases such as Hutchinson-Gilford progeria syndrome (HGPS) and various tumors, with serious consequences. Remodelin, an inhibitor of NAT10, delays HGPS progression; many studies have been conducted on its role in tumor therapy. A major breakthrough in the study of NAT10 was the discovery of mRNA N4-acetylcytidine (ac4C) modification, which can increase mRNA stability and translation efficiency significantly. In addition, NAT10 modifies the mRNA of ac4C, which is associated with tumor development. Here, we present a review of pertinent studies focusing on NAT10, particularly its role in cancer, to provide researchers with a concise and informative summary of the current state of knowledge about this topic. The conclusions drawn from this review could provide a new direction for tumor treatment.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Limite: Animals / Humans Idioma: En Revista: Discov Med Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Neoplasias Limite: Animals / Humans Idioma: En Revista: Discov Med Ano de publicação: 2024 Tipo de documento: Article