SETD4 inhibits prostate cancer development by promoting H3K27me3-mediated NUPR1 transcriptional repression and cell cycle arrest

Wang, Chong; Wang, Tao; Li, Kang-Jing; Hu, Ling-Hong; Li, Yue; Yu, Yu-Zhong; Xie, Tao; Zhu, Sha; Fu, Du-Jiang; Wang, Yang; Zeng, Xian-Zi; Liu, Feng-Ping; Chen, Hong; Chen, Zhe-Sheng; Feng, Ning-Han; Liu, Jinghua; Jiang, Yong; Zhao, Shan-Chao

doi:10.1016/j.canlet.2023.216464

Cancer Letters

2023

DOI: 10.1016/j.canlet.2023.216464

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SETD4 inhibits prostate cancer development by promoting H3K27me3-mediated NUPR1 transcriptional repression and cell cycle arrest

Chong Wang,

Tao Wang,

Kang-Jing Li

et al.

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2024

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Cited by 5 publications

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NAT10 Promotes Prostate Cancer Growth and Metastasis by Acetylating mRNAs of HMGA1 and KRT8

Li,

Hong,

et al. 2024

Advanced Science

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N4‐acetylcytidine (ac4C) is essential for the development and migration of tumor cells. According to earlier research, N‐acetyltransferase 10 (NAT10) can increase messenger RNAs (mRNAs) stability by catalyzing the synthesis of ac4C. However, little is known about NAT10 expression and its role in the acetylation modifications in prostate cancer (PCa). Thus, the biological function of NAT10 in PCa is investigated in this study. Compared to paraneoplastic tissues, the expression of NAT10 is significantly higher in PCa. The NAT10 expression is strongly correlated with the pathological grade, clinical stage, Gleason score, T‐stage, and N‐stage of PCa. NAT10 has the ability to advance the cell cycle and the epithelial‐mesenchymal transition (EMT), both of which raise the malignancy of tumor cells. Mechanistically, NAT10 enhance the stability of high mobility group AT‐hook 1 (HMGA1) by acetylating its mRNA, thereby promoting cell cycle progression to improve cell proliferation. In addition, NAT10 improve the stability of Keratin 8 (KRT8) by acetylating its mRNA, which promotes the progression of EMT to improve cell migration. This findings provide a potential prognostic or therapeutic target for PCa.

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NAT10 Promotes Prostate Cancer Growth and Metastasis by Acetylating mRNAs of HMGA1 and KRT8

Li,

Hong,

et al. 2024

Advanced Science

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The role and mechanism of NAT10‐mediated ac4C modification in tumor development and progression

Gu,

Zou,

Pan

et al. 2024

MedComm

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RNA modification has emerged as a crucial area of research in epigenetics, significantly influencing tumor biology by regulating RNA metabolism. N‐acetyltransferase 10 (NAT10)‐mediated N4‐acetylcytidine (ac4C) modification, the sole known acetylation in eukaryotic RNA, influences cancer pathogenesis and progression. NAT10 is the only writer of ac4C and catalyzes acetyl transfer on targeted RNA, and ac4C helps to improve the stability and translational efficiency of ac4C‐modified RNA. NAT10 is highly expressed and associated with poor prognosis in pan‐cancers. Based on its molecular mechanism and biological functions, ac4C is a central factor in tumorigenesis, tumor progression, drug resistance, and tumor immune escape. Despite the increasing focus on ac4C, the specific regulatory mechanisms of ac4C in cancer remain elusive. The present review thoroughly analyzes the current knowledge on NAT10‐mediated ac4C modification in cancer, highlighting its broad regulatory influence on targeted gene expression and tumor biology. This review also summarizes the limitations and perspectives of current research on NAT10 and ac4C in cancer, to identify new therapeutic targets and advance cancer treatment strategies.

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Evaluation of glucocorticoid-related genes reveals GPD1 as a therapeutic target and regulator of sphingosine 1-phosphate metabolism in CRPC

Liu,

Zou,

Zhang

et al. 2024

Cancer Letters

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SETD4 inhibits prostate cancer development by promoting H3K27me3-mediated NUPR1 transcriptional repression and cell cycle arrest

Cited by 5 publications

References 54 publications

NAT10 Promotes Prostate Cancer Growth and Metastasis by Acetylating mRNAs of HMGA1 and KRT8

NAT10 Promotes Prostate Cancer Growth and Metastasis by Acetylating mRNAs of HMGA1 and KRT8

The role and mechanism of NAT10‐mediated ac4C modification in tumor development and progression

Evaluation of glucocorticoid-related genes reveals GPD1 as a therapeutic target and regulator of sphingosine 1-phosphate metabolism in CRPC

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