The role of DUBs in the post-translational control of cell migration

Lambies, Guillem; Herreros, Antonio Garcı́a de; Dı́az, Vı́ctor M.

doi:10.1042/ebc20190022

Cited by 8 publications

(6 citation statements)

References 173 publications

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“…The stability of EMT-related transcription factors is essential for initiating cellular EMT. Thus, the deubiquitinases (DUBs) were involved in counteracting polyubiquitination and proteasomal degradation of ZEB1 [40]; these DUBs include USP51, which upregulated ZEB1 and the mesenchymal markers by binding, deubiquitinating, and stabilizing ZEB1 [41]. In addition to DUBs, other factors, such as CSN5, an oncogene involved in various types of cancer, may also interrupt the degradation of ZEB1 by stabilizing ZEB1 by directly interacting with it [42].…”

Section: The Regulation Of Zeb1 Expression and Activitymentioning

confidence: 99%

Oncogenic functions of the EMT-related transcription factor ZEB1 in breast cancer

Zhong

et al. 2020

J Transl Med

105

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Zinc finger E-box binding homeobox 1 (ZEB1, also termed TCF8 and δEF1) is a crucial member of the zinc fingerhomeodomain transcription factor family, originally identified as a binding protein of the lens-specific δ1-crystalline enhancer and is a pivotal transcription factor in the epithelial-mesenchymal transition (EMT) process. ZEB1 also plays a vital role in embryonic development and cancer progression, including breast cancer progression. Increasing evidence suggests that ZEB1 stimulates tumor cells with mesenchymal traits and promotes multidrug resistance, proliferation, and metastasis, indicating the importance of ZEB1-induced EMT in cancer development. ZEB1 expression is regulated by multiple signaling pathways and components, including TGF-β, β-catenin, miRNA and other factors. Here, we summarize the recent discoveries of the functions and mechanisms of ZEB1 to understand the role of ZEB1 in EMT regulation in breast cancer.

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Section: The Regulation Of Zeb1 Expression and Activitymentioning

confidence: 99%

Oncogenic functions of the EMT-related transcription factor ZEB1 in breast cancer

Zhong

et al. 2020

J Transl Med

105

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“…Acute myeloid leukemia MSCs promoted the mRNA level of Snail1 but inhibited its protein expression; this does not conform to classical EMT regulation. It has been reported that Snail1 protein is unstable and controlled by a specific type of protease 32 . Acute myeloid leukemia MSCs also promoted the mRNA levels of Twist1 and vimentin in K562 cells and HL60 cells, but had the opposite or little effect on relevant protein expressions in K562 cells and HL60 cells, respectively.…”

Section: Discussionmentioning

confidence: 93%

“…It has been reported that Snail1 protein is unstable and controlled by a specific type of protease. 32 Acute myeloid leukemia MSCs also promoted the mRNA levels of Twist1 and vimentin in K562 cells and HL60 cells, but had the opposite or little effect on relevant protein expressions in K562 cells and HL60 cells, respectively. It had been reported that EMT is dynamic and not a binary process, depending on the cell type and tissue type.…”

Section: Discussionmentioning

confidence: 95%

Acute myeloid leukemia (AML)‐derived mesenchymal stem cells induce chemoresistance and epithelial–mesenchymal transition‐like program in AML through IL‐6/JAK2/STAT3 signaling

Dong

Zhang

et al. 2023

Cancer Science

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Acute myeloid leukemia (AML) has a high rate of treatment failure due to increased prevalence of therapy resistance. Mesenchymal stem cells (MSCs) in the leukemia microenvironment contribute to chemoresistance in AML, but the specific mechanism remains unclear. The critical role of the epithelial-mesenchymal transition (EMT)-like profile in AML chemoresistance has been gradually recognized. However, there is no research to suggest that the AML-derived bone marrow mesenchymal stem cells

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“… 26 More evidence indicates that USP17 subfamily proteins may regulate EMT of various cells by acting on Snail1, Snail2, and Twist1. 27 …”

Section: Discussionmentioning

confidence: 99%

Exploring the Molecular Mechanism of lncRNA–miRNA–mRNA Networks in Non-Syndromic Cleft Lip with or without Cleft Palate

Wang¹,

Guo²,

Zhou³

et al. 2021

IJGM

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Background Non-syndromic cleft lip with or without cleft palate (NSCL/P) is a common craniofacial birth defect. Growing evidence has demonstrated the competing endogenous RNA (ceRNA) hypothesis has played a role in the pathogenesis of NSCL/P. Here, we identified the important lncRNAs in NSCL/P and constructed a ceRNA regulatory network to predict their underlying functional mechanism. Methods Total RNA isolated from the peripheral blood samples were analyzed by the Human Clariom D Affymetrix platform and differentially expressed genes (DEGs) were identified. Using the limma package in R software, DEGs in the expression profile of GSE42589 were identified from Gene Expression Omnibus (GEO) database. Co-differentially expressed lncRNAs (co-DElncRNAs) were used to predict the microRNAs that may bind to them. Co-differentially expressed mRNAs (co-DEmRNAs) were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. The hub genes were screened using the cytohubba plug-in in Cytoscape. A ceRNA network was built to investigate the molecular mechanism underlying the etiology of NSCL/P. The expression levels of lncRNAs, miRNAs, and mRNAs in the network were assessed by quantitative real-time polymerase chain reaction (qRT-PCR). Results We found 116 DElncRNAs and 2955 DEmRNAs from the GSE42589 dataset, and 2626 DElncRNAs and 2771 DEmRNAs from the Human Clariom D gene chip. A network of co-DEmRNAs containing 3712 edges and 621 nodes were identified by PPI analysis. A ceRNA regulatory network comprising lncRNA USP17L6P, hsa-miR-449c-5p, and MYC was established. qRT-PCR results revealed significantly lower expression levels of lncRNA USP17L6P and c-Myc in NSCL/P tissues, while the expression level of hsa-miR-449c-5p was higher as compared to control samples ( p < 0.05). Conclusion The identified lncRNAs and the established ceRNA regulatory network provide novel insight into the pathogenesis of NSCL/P, therefore hold great promise in NSCL/P management in clinical practice.

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The role of DUBs in the post-translational control of cell migration

Cited by 8 publications

References 173 publications

Oncogenic functions of the EMT-related transcription factor ZEB1 in breast cancer

Oncogenic functions of the EMT-related transcription factor ZEB1 in breast cancer

Acute myeloid leukemia (AML)‐derived mesenchymal stem cells induce chemoresistance and epithelial–mesenchymal transition‐like program in AML through IL‐6/JAK2/STAT3 signaling

Exploring the Molecular Mechanism of lncRNA–miRNA–mRNA Networks in Non-Syndromic Cleft Lip with or without Cleft Palate

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