A Review of Research on the Mechanism of Tumor Regulation by N-Acetyltransferase 10.

Discov Med

The Department of General Surgery, The First Hospital of Lanzhou University, 730000 Lanzhou, Gansu, China.

Published: July 2024

AI Article Synopsis

  • N-acetyltransferase 10 (NAT10) is crucial for various cellular processes, including regulating telomerase activity and participating in DNA damage response, and its dysfunction can lead to serious conditions like Hutchinson-Gilford progeria syndrome and tumors.
  • Remodelin, a NAT10 inhibitor, has shown potential in slowing HGPS progression and is being investigated for its effects in cancer therapy.
  • The recent discovery of NAT10's role in mRNA N4-acetylcytidine (ac4C) modification, which enhances mRNA stability and translation efficiency, highlights its significance in tumor development and opens new avenues for cancer treatment research.

Article 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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Source
http://dx.doi.org/10.24976/Discov.Med.202436186.123DOI Listing

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