Death-associated protein 3 in cell death and beyond

Cao, Ting; Luo, Xuling; Zheng, Binjiao; Deng, Yao; Zhang, Yu; Li, Yuyan; Xi, Wenwen; Guo, Meng; Yang, Xuefeng; Li, Zhiyue; Lu, Bin

doi:10.1007/s42764-024-00125-9

Cited by 2 publications

(1 citation statement)

References 69 publications

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“…Recently, we found that the loss of nhr-14 gene in c. elegans resulted in the dysregulation of DNA damage-induced response [14], which usually leads to cancer development [15][16][17][18]. Thus, we examined HNF4α expression levels in different cancers and matched paired normal tissues.…”

Section: Hnf4 α Promotes Colorectal Carcinogenesismentioning

confidence: 99%

HNF4α is a target of the Wnt/β-catenin pathway and regulates colorectal carcinogenesis

Sang,

Bai,

et al. 2024

Preprint

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Hepatocyte nuclear factor 4alpha (HNFalpha) is a transcription factor involved in liver function. Dysregulation of HNF4alpha leads to hepatocarcinogenesis. However, the role and mechanism of HNF4alpha; in colorectal cancer is still unknown. Here we demonstrate that HNF4alpha is upregulated in colorectal cancers. and HNF4alpha upregulation promotes colorectal tumorigenesis. Notably, expression levels of HNF4alpha are positively correlated with the Wnt/beta-catenin signaling pathway in colorectal cancer patients. Further, we showed that HNF4alpha is transcriptionally activated by Wnt/beta-catenin/TCF3 and is at least partially responsible for the oncognesis activity of the Wnt signaling in colorectal cancer. Our findings indicate that HNF4alpha is a direct target of that Wnt/beta-catenin pathway and could play an important role in colorectal carcinogenesis.

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Section: Hnf4 α Promotes Colorectal Carcinogenesismentioning

confidence: 99%

HNF4α is a target of the Wnt/β-catenin pathway and regulates colorectal carcinogenesis

Sang,

Bai,

et al. 2024

Preprint

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Modulation of m ⁶ A RNA modification by DAP3 in cancer cells

Han,

Song,

Xie

et al. 2024

Proc. Natl. Acad. Sci. U.S.A.

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N 6 -methyladenosine (m 6 A) RNA methylation is a prevalent RNA modification that significantly impacts RNA metabolism and cancer development. Maintaining the global m 6 A levels in cancer cells relies on RNA accessibility to methyltransferases and the availability of the methyl donor S-adenosylmethionine (SAM). Here, we reveal that death associated protein 3 (DAP3) plays a crucial role in preserving m 6 A levels through two distinct mechanisms. First, although DAP3 is not a component of the m 6 A writer complex, it directly binds to m 6 A target regions, thereby facilitating METTL3 binding. Second, DAP3 promotes MAT2A ’s last intron splicing, increasing MAT2A protein, cellular SAM, and m 6 A levels. Silencing DAP3 hinders tumorigenesis, which can be rescued by MAT2A overexpression. This evidence suggests DAP3’s role in tumorigenesis, partly through m 6 A regulation. Our findings unveil DAP3’s complex role as an RNA-binding protein and tumor promoter, impacting RNA processing, splicing, and m 6 A modification in cancer transcriptomes.

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Death-associated protein 3 in cell death and beyond

Cited by 2 publications

References 69 publications

HNF4α is a target of the Wnt/β-catenin pathway and regulates colorectal carcinogenesis

HNF4α is a target of the Wnt/β-catenin pathway and regulates colorectal carcinogenesis

Modulation of m ⁶ A RNA modification by DAP3 in cancer cells

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Death-associated protein 3 in cell death and beyond

Cited by 2 publications

References 69 publications

HNF4α is a target of the Wnt/β-catenin pathway and regulates colorectal carcinogenesis

HNF4α is a target of the Wnt/β-catenin pathway and regulates colorectal carcinogenesis

Modulation of m 6 A RNA modification by DAP3 in cancer cells

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Product

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Modulation of m ⁶ A RNA modification by DAP3 in cancer cells