The repression of oncoprotein SET by the tumor suppressor p53 reveals a p53-SET-PP2A feedback loop for cancer therapy

Yao, Han; Xu, Wenbin; Liu, Yajing; Cao, Zhijie; Wen, Jia; Zhang, Mi; Wu, Zhen; Jiao, Zishan; Zhang, Zijing; Chen, Jianyuan; Zhang, Meng; Zhu, Weiguo; Wang, Donglai

doi:10.1007/s11427-021-2123-8

Cited by 5 publications

(4 citation statements)

References 33 publications

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“…Furthermore, Yang et al. (2023) discovered the emergence of a significant collection of novel genes in cotton owing to long terminal repeat insertions, which had not been extensively identified in prior genome assemblies and annotations.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies have also identified transposable insertions within introns that affect phenotypes through gene expression in rapeseed (Jin et al, 2022) and maize (Zhong et al, 2021). Furthermore, Yang et al (2023) discovered the emergence of a significant collection of novel genes in cotton owing to long terminal repeat insertions, which had not been extensively identified in prior genome assemblies and annotations.…”

Section: Discussionmentioning

confidence: 99%

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R2R3‐MYB transcription factor CsMYB60 controls mature fruit skin color by regulating flavonoid accumulation in cucumber

Xu,

Zhu,

Yuan

et al. 2024

The Plant Journal

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SUMMARYSkin color is an important trait that determines the cosmetic appearance and quality of fruits. In cucumber, the skin color ranges from white to brown in mature fruits. However, the genetic basis for this important trait remains unclear. We conducted a genome‐wide association study of natural cucumber populations, along with map‐based cloning techniques, on an F2 population resulting from a cross between Pepino (with yellow‐brown fruit skin) and Zaoer‐N (with creamy fruit skin). We identified CsMYB60 as a candidate gene responsible for skin coloration in mature cucumber fruits. In cucumber accessions with white to pale yellow skin color, a premature stop mutation (C to T) was found in the second exon region of CsMYB60, whereas light yellow cucumber accessions exhibited splicing premature termination caused by an intronic mutator‐like element insertion in CsMYB60. Transgenic CsMYB60c cucumber plants displayed a yellow‐brown skin color by promoting accumulation of flavonoids, especially hyperoside, a yellow‐colored flavonol. CsMYB60c encodes a nuclear protein that primarily acts as a transcriptional activator through its C‐terminal activation motif. RNA sequencing and DNA affinity purification sequencing assays revealed that CsMYB60c promotes skin coloration by directly binding to the YYTACCTAMYT motif in the promoter regions of flavonoid biosynthetic genes, including CsF3′H, which encodes flavonoid 3′‐hydroxylase. The findings of our study not only offer insight into the function of CsMYB60 as dominantly controlling fruit coloration, but also highlight that intronic DNA mutations can have a similar phenotypic impact as exonic mutations, which may be valuable in future cucumber breeding programs.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

R2R3‐MYB transcription factor CsMYB60 controls mature fruit skin color by regulating flavonoid accumulation in cucumber

Xu,

Zhu,

Yuan

et al. 2024

The Plant Journal

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“…Thus, the oncoprotein SET links the modulation of two key tumor suppressive pathways, p53 and PP2A ( Figure 4 ). According to preclinical studies, p53 activation and SET antagonism exert a significant synergistic effect on tumor suppression ( Yao et al., 2023 ).…”

Section: Intracellular Regulation Of Setmentioning

confidence: 99%

The next decade of SET: from an oncoprotein to beyond

Yao,

Zhang,

Wang

2023

Journal of Molecular Cell Biology

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This year marks the fourth decade of research into the protein SET, which was discovered in 1992. SET was initially identified as an oncoprotein, but later, it was shown to be a multifaceted protein involved in regulating numerous biological processes under both physiological and pathophysiological conditions. SET dysfunction is closely associated with diseases, such as cancer and Alzheimer's disease. With the increasing understanding of how SET works and how it is regulated in cells, targeting aberrant SET has emerged as a potential strategy for disease intervention. In this review, we present a comprehensive overview of the advancements in SET studies, encompassing its biological functions, regulatory networks, clinical implications, and pharmacological inhibitors. Furthermore, we provide insights into the future prospects of SET research, with a particular emphasis on its promising potential in the realm of immune modulation.

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“…In addition, nuclear SET mainly serves as a chaperone that intimately associates with histones for nucleosome assembly or acts as a cofactor that binds transcription factors (TFs) for gene-specific transcriptional regulation 6 , 17 , 18 . Thus, targeting aberrant SET by individual or combined strategies may trigger both cytoplasm- and nucleus-involved mechanisms for tumor, including lung carcinoma, intervention 12 , 19 . However, the major TFs within the nucleus dictating SET for metastatic regulation in lung cancer are still obscure.…”

Section: Introductionmentioning

confidence: 99%

Oncoprotein SET-associated transcription factor ZBTB11 triggers lung cancer metastasis

Xu,

Yao,

et al. 2024

Nat Commun

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Metastasis is the major cause of lung cancer-related death, but the mechanisms governing lung tumor metastasis remain incompletely elucidated. SE translocation (SET) is overexpressed in lung tumors and correlates with unfavorable prognosis. Here we uncover SET-associated transcription factor, zinc finger and BTB domain-containing protein 11 (ZBTB11), as a prometastatic regulator in lung tumors. SET interacts and collaborates with ZBTB11 to promote lung cancer cell migration and invasion, primarily through SET-ZBTB11 complex-mediated transcriptional activation of matrix metalloproteinase-9 (MMP9). Additionally, by transcriptional repression of proline-rich Gla protein 2 (PRRG2), ZBTB11 links Yes-associated protein 1 (YAP1) activation to drive lung tumor metastasis independently of SET-ZBTB11 complex. Loss of ZBTB11 suppresses distal metastasis in a lung tumor mouse model. Overexpression of ZBTB11 is recapitulated in human metastatic lung tumors and correlates with diminished survival. Our study demonstrates ZBTB11 as a key metastatic regulator and reveals diverse mechanisms by which ZBTB11 modulates lung tumor metastasis.

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The repression of oncoprotein SET by the tumor suppressor p53 reveals a p53-SET-PP2A feedback loop for cancer therapy

Cited by 5 publications

References 33 publications

R2R3‐MYB transcription factor CsMYB60 controls mature fruit skin color by regulating flavonoid accumulation in cucumber

R2R3‐MYB transcription factor CsMYB60 controls mature fruit skin color by regulating flavonoid accumulation in cucumber

The next decade of SET: from an oncoprotein to beyond

Oncoprotein SET-associated transcription factor ZBTB11 triggers lung cancer metastasis

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