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Article ; Online: The epigenetic roles of DNA N

Wu, Kou-Juey

2020 Volume 494, Page(s) 40–46

Abstract: ... The DNA ... ...

Abstract	The DNA N
MeSH term(s)	Adenine/analogs & derivatives ; Adenine/metabolism ; Animals ; DNA/metabolism ; DNA Methylation ; Epigenesis, Genetic ; Gene Expression Regulation ; Plants/genetics
Chemical Substances	DNA (9007-49-2) ; Adenine (JAC85A2161) ; 6-methyladenine (W7IBY2BGAX)
Language	English
Publishing date	2020-08-23
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2020.08.025
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Article ; Online: The role of miRNA biogenesis and DDX17 in tumorigenesis and cancer stemness.

Wu, Kou-Juey

Biomedical journal

2020 Volume 43, Issue 2, Page(s) 107–114

Abstract: Cancer stemness represents one of the major mechanisms that predispose patients to tumor aggressiveness, metastasis, and treatment resistance. MicroRNA biogenesis is an important process controlling miRNA processing and maturation. Deregulation of miRNA ... ...

Abstract	Cancer stemness represents one of the major mechanisms that predispose patients to tumor aggressiveness, metastasis, and treatment resistance. MicroRNA biogenesis is an important process controlling miRNA processing and maturation. Deregulation of miRNA biogenesis can lead to tumorigenesis and cancer stemness. DDX17 is a co-factor of the miRNA microprocessor. Misregulation of DDX17 can be associated with cancer stemness. K63-linked polyubiquitination of DDX17 presents a concerted mechanism of decreased synthesis of stemness-inhibiting miRNAs and increased transcriptional activation of stemness-related gene expression. K63-linked polyubiquitination of HAUSP serves as a scaffold to anchor HIF-1α, CBP, the mediator complex, and the super-elongation complex to enhance HIF-1α-induced gene transcription. Recent progress in RNA modifications shows that RNA N6-methyladenosine (m6A) modification is a crucial mechanism to regulate RNA levels. M6A modification of miRNAs can also be linked to tumorigenesis and cancer stemness. Overall, miRNA biogenesis and K63-linked polyubiquitination of DDX17 play an important role in the induction of cancer stemness. Delineation of the mechanisms and identification of suitable targets may provide new therapeutic options for treatment-resistant cancers.
MeSH term(s)	Cell Transformation, Neoplastic/genetics ; DEAD-box RNA Helicases/genetics ; DEAD-box RNA Helicases/metabolism ; Humans ; MicroRNAs/genetics ; Neoplastic Stem Cells ; Signal Transduction/genetics
Chemical Substances	MicroRNAs ; DDX17 protein, human (EC 3.6.1.-) ; DEAD-box RNA Helicases (EC 3.6.4.13)
Language	English
Publishing date	2020-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2698541-X
ISSN	2320-2890 ; 2320-2890
ISSN (online)	2320-2890
ISSN	2320-2890
DOI	10.1016/j.bj.2020.03.001
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: The role of miRNA biogenesis and DDX17 in tumorigenesis and cancer stemness

Kou-Juey Wu

Biomedical Journal, Vol 43, Iss 2, Pp 107-

2020 Volume 114

Abstract	Cancer stemness represents one of the major mechanisms that predispose patients to tumor aggressiveness, metastasis, and treatment resistance. MicroRNA biogenesis is an important process controlling miRNA processing and maturation. Deregulation of miRNA biogenesis can lead to tumorigenesis and cancer stemness. DDX17 is a co-factor of the miRNA microprocessor. Misregulation of DDX17 can be associated with cancer stemness. K63-linked polyubiquitination of DDX17 presents a concerted mechanism of decreased synthesis of stemness-inhibiting miRNAs and increased transcriptional activation of stemness-related gene expression. K63-linked polyubiquitination of HAUSP serves as a scaffold to anchor HIF-1α, CBP, the mediator complex, and the super-elongation complex to enhance HIF-1α-induced gene transcription. Recent progress in RNA modifications shows that RNA N6-methyladenosine (m6A) modification is a crucial mechanism to regulate RNA levels. M6A modification of miRNAs can also be linked to tumorigenesis and cancer stemness. Overall, miRNA biogenesis and K63-linked polyubiquitination of DDX17 play an important role in the induction of cancer stemness. Delineation of the mechanisms and identification of suitable targets may provide new therapeutic options for treatment-resistant cancers.
Keywords	miRNA biogenesis ; DDX17 ; Cancer stemness ; HAUSP ; K63-linked polyubiquitination ; m6A ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2020-04-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: A refined Uni-vector prime editing system improves genome editing outcomes in mammalian cells.

Huang, Ching-Hui / Chiu, Szu-Ying / Chou, Yu-Chi / Wu, Kou-Juey

Biotechnology journal

2023 Volume 19, Issue 2, Page(s) e2300353

Abstract: Prime editing is an advanced technology in CRISPR/Cas research with increasing numbers of improved methodologies. The original multi-vector method hampers the efficiency and precision of prime editing and also has inherent difficulty in generating ... ...

Abstract	Prime editing is an advanced technology in CRISPR/Cas research with increasing numbers of improved methodologies. The original multi-vector method hampers the efficiency and precision of prime editing and also has inherent difficulty in generating homozygous mutations in mammalian cells. To overcome these technical issues, we developed a Uni-vector prime editing system, wherein the major components for prime editing were constructed in all-in-one plasmids, pPE3-pPuro and pePEmax-pPuro. The Uni-vector prime editing plasmids enhance the editing efficiency of prime editing and improved the generation of homozygous mutated mammalian cell lines. The editing efficiency is dependent of the transfection efficiency. Remarkably, the Uni-vector ePE5max system achieved an impressive editing rate approximately 79% in average, even in cell lines that are traditionally difficult to transfect, such as FaDu cell line. Furthermore, it resulted in a high frequency of homozygous knocked-in cells, with a rate of 99% in HeLa and 85% in FaDu cells. Together, our Uni-vector approach simplifies the delivery of editing components and improves the editing efficiency, especially in cells with low transfection efficiency. This approach presents an advancement in the field of prime editing.
MeSH term(s)	Animals ; Humans ; Gene Editing ; HeLa Cells ; Mutation ; Transfection ; CRISPR-Cas Systems/genetics ; Mammals
Language	English
Publishing date	2023-12-16
Publishing country	Germany
Document type	Journal Article
ZDB-ID	2221885-3
ISSN	1860-7314 ; 1860-6768
ISSN (online)	1860-7314
ISSN	1860-6768
DOI	10.1002/biot.202300353
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Article ; Online: Organ defects of the Usp7K444R mutant mouse strain indicate the essential role of K63-polyubiquitinated Usp7 in organ formation

Han-Tsang Wu / Yueh-Te Lin / Shan Hwu Chew / Kou-Juey Wu

Biomedical Journal, Vol 46, Iss 1, Pp 122-

2023 Volume 133

Abstract: Background: K63-linked polyubiquitination of proteins have nonproteolytic functions and regulate the activity of many signal transduction pathways. USP7, a HIF1α deubiquitinase, undergoes K63-linked polyubiquitination under hypoxia. K63-polyubiquitinated ...

Abstract	Background: K63-linked polyubiquitination of proteins have nonproteolytic functions and regulate the activity of many signal transduction pathways. USP7, a HIF1α deubiquitinase, undergoes K63-linked polyubiquitination under hypoxia. K63-polyubiquitinated USP7 serves as a scaffold to anchor HIF1α, CREBBP, the mediator complex, and the super elongation complex to enhance HIF1α-induced gene transcription. However, the physiological role of K63-polyubiquitinated USP7 remains unknown. Methods: Using a Usp7K444R point mutation knock-in mouse strain, we performed immunohistochemistry and standard molecular biological methods to examine the organ defects of liver and kidney in this knock-in mouse strain. Mechanistic studies were performed by using deubiquitination, immunoprecipitation, and quantitative immunoprecipitations (qChIP) assays. Results: We observed multiple organ defects, including decreased liver and muscle weight, decreased tibia/fibula length, liver glycogen storage defect, and polycystic kidneys. The underlying mechanisms include the regulation of protein stability and/or modulation of transcriptional activation of several key factors, leading to decreased protein levels of Prr5l, Hnf4α, Cebpα, and Hnf1β. Repression of these crucial factors leads to the organ defects described above. Conclusions: K63-polyubiquitinated Usp7 plays an essential role in the development of multiple organs and illustrates the importance of the process of K63-linked polyubiquitination in regulating critical protein functions.
Keywords	Usp7 ; K63-linked polyubiquitination ; Knock-in mouse ; Glycogen storage ; Polycystic kidney ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
Subject code	571
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
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Article ; Online: Epigenetic regulation of epithelial-mesenchymal transition: focusing on hypoxia and TGF-β signaling.

Lin, Yueh-Te / Wu, Kou-Juey

Journal of biomedical science

2020 Volume 27, Issue 1, Page(s) 39

Abstract: Epithelial-mesenchymal transition (EMT) is an important process triggered during cancer metastasis. Regulation of EMT is mostly initiated by outside signalling, including TGF-β, growth factors, Notch ligand, Wnt, and hypoxia. Many signalling pathways ... ...

Abstract	Epithelial-mesenchymal transition (EMT) is an important process triggered during cancer metastasis. Regulation of EMT is mostly initiated by outside signalling, including TGF-β, growth factors, Notch ligand, Wnt, and hypoxia. Many signalling pathways have been delineated to explain the molecular mechanisms of EMT. In this review, we will focus on the epigenetic regulation of two critical EMT signalling pathways: hypoxia and TGF-β. For hypoxia, hypoxia-induced EMT is mediated by the interplay between chromatin modifiers histone deacetylase 3 (HDAC3) and WDR5 coupled with the presence of histone 3 lysine 4 acetylation (H3K4Ac) mark that labels the promoter regions of various traditional EMT marker genes (e.g. CDH1, VIM). Recently identified new hypoxia-induced EMT markers belong to transcription factors (e.g. SMO, GLI1) that mediate EMT themselves. For TGF-β-induced ΕΜΤ, global chromatin changes, removal of a histone variant (H2A.Z), and new chromatin modifiers (e.g. UTX, Rad21, PRMT5, RbBP5, etc) are identified to be crucial for the regulation of both EMT transcription factors (EMT-TFs) and EMT markers (EMT-Ms). The epigenetic mechanisms utilized in these two pathways may serve as good model systems for other signalling pathways and also provide new potential therapeutic targets.
MeSH term(s)	Epigenesis, Genetic ; Epithelial-Mesenchymal Transition/genetics ; Humans ; Hypoxia/genetics ; Signal Transduction ; Transforming Growth Factor beta/genetics ; Transforming Growth Factor beta/metabolism
Chemical Substances	Transforming Growth Factor beta
Language	English
Publishing date	2020-03-02
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1193378-1
ISSN	1423-0127 ; 1021-7770
ISSN (online)	1423-0127
ISSN	1021-7770
DOI	10.1186/s12929-020-00632-3
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Zs.A 4037: Show issues

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Article ; Online: Organ defects of the Usp7

Wu, Han-Tsang / Lin, Yueh-Te / Chew, Shan Hwu / Wu, Kou-Juey

Biomedical journal

2022 Volume 46, Issue 1, Page(s) 122–133

Abstract	Background: K63-linked polyubiquitination of proteins have nonproteolytic functions and regulate the activity of many signal transduction pathways. USP7, a HIF1α deubiquitinase, undergoes K63-linked polyubiquitination under hypoxia. K63-polyubiquitinated USP7 serves as a scaffold to anchor HIF1α, CREBBP, the mediator complex, and the super elongation complex to enhance HIF1α-induced gene transcription. However, the physiological role of K63-polyubiquitinated USP7 remains unknown. Methods: Using a Usp7 Results: We observed multiple organ defects, including decreased liver and muscle weight, decreased tibia/fibula length, liver glycogen storage defect, and polycystic kidneys. The underlying mechanisms include the regulation of protein stability and/or modulation of transcriptional activation of several key factors, leading to decreased protein levels of Prr5l, Hnf4α, Cebpα, and Hnf1β. Repression of these crucial factors leads to the organ defects described above. Conclusions: K63-polyubiquitinated Usp7 plays an essential role in the development of multiple organs and illustrates the importance of the process of K63-linked polyubiquitination in regulating critical protein functions.
MeSH term(s)	Mice ; Animals ; Ubiquitin-Specific Peptidase 7/genetics ; Ubiquitin-Specific Peptidase 7/metabolism ; Ubiquitination ; Mice, Mutant Strains ; Kidney/metabolism ; Signal Transduction
Chemical Substances	Ubiquitin-Specific Peptidase 7 (EC 3.4.19.12)
Language	English
Publishing date	2022-02-18
Publishing country	United States
Document type	Journal Article
ZDB-ID	2698541-X
ISSN	2320-2890 ; 2320-2890
ISSN (online)	2320-2890
ISSN	2320-2890
DOI	10.1016/j.bj.2022.02.002
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Article: Liquid-liquid phase separation (LLPS) in cellular physiology and tumor biology.

Peng, Pei-Hua / Hsu, Kai-Wen / Wu, Kou-Juey

American journal of cancer research

2021 Volume 11, Issue 8, Page(s) 3766–3776

Abstract: Liquid-liquid phase separation (LLPS) has emerged as a mechanism that has been used to explain the formation of known organelles (e.g. nucleoli, promyelocytic leukemia nuclear bodies (PML NBs), etc) as well as other membraneless condensates (e.g. ... ...

Abstract	Liquid-liquid phase separation (LLPS) has emerged as a mechanism that has been used to explain the formation of known organelles (e.g. nucleoli, promyelocytic leukemia nuclear bodies (PML NBs), etc) as well as other membraneless condensates (e.g. nucleosome arrays, DNA damage foci, X-chromosome inactivation (XCI) center, paraspeckles, stress granules, proteasomes, autophagosomes, etc). The formation of membraneless condensates could be triggered by proteins containing modular domains or intrinsically disordered regions (IDRs) and nucleic acids. Multiple biological processes including transcription, chromatin organization, X-chromosome inactivation (XCI), DNA damage, tumorigenesis, autophagy, etc have been shown to utilize the principle of LLPS to facilitate these processes. This review will summarize the principle and components of LLPS, and describe how LLPS regulate these numerous biological processes and disruption of LLPS would cause disease formation. The role of LLPS in regulating normal cellular physiology and contributing to tumorigenesis will be discussed.
Language	English
Publishing date	2021-08-15
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2589522-9
ISSN	2156-6976
ISSN	2156-6976
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Article ; Online: Epigenetic regulation of epithelial-mesenchymal transition

Yueh-Te Lin / Kou-Juey Wu

Journal of Biomedical Science, Vol 27, Iss 1, Pp 1-

focusing on hypoxia and TGF-β signaling

2020 Volume 10

Abstract: Abstract Epithelial-mesenchymal transition (EMT) is an important process triggered during cancer metastasis. Regulation of EMT is mostly initiated by outside signalling, including TGF-β, growth factors, Notch ligand, Wnt, and hypoxia. Many signalling ... ...

Abstract	Abstract Epithelial-mesenchymal transition (EMT) is an important process triggered during cancer metastasis. Regulation of EMT is mostly initiated by outside signalling, including TGF-β, growth factors, Notch ligand, Wnt, and hypoxia. Many signalling pathways have been delineated to explain the molecular mechanisms of EMT. In this review, we will focus on the epigenetic regulation of two critical EMT signalling pathways: hypoxia and TGF-β. For hypoxia, hypoxia-induced EMT is mediated by the interplay between chromatin modifiers histone deacetylase 3 (HDAC3) and WDR5 coupled with the presence of histone 3 lysine 4 acetylation (H3K4Ac) mark that labels the promoter regions of various traditional EMT marker genes (e.g. CDH1, VIM). Recently identified new hypoxia-induced EMT markers belong to transcription factors (e.g. SMO, GLI1) that mediate EMT themselves. For TGF-β-induced ΕΜΤ, global chromatin changes, removal of a histone variant (H2A.Z), and new chromatin modifiers (e.g. UTX, Rad21, PRMT5, RbBP5, etc) are identified to be crucial for the regulation of both EMT transcription factors (EMT-TFs) and EMT markers (EMT-Ms). The epigenetic mechanisms utilized in these two pathways may serve as good model systems for other signalling pathways and also provide new potential therapeutic targets.
Keywords	Epithelial-mesenchymal transition ; Hypoxia ; TGF-β ; Epigenetic regulation ; HIF-1α ; HDAC3 ; Medicine ; R
Subject code	570
Language	English
Publishing date	2020-03-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article ; Online: Epigenetic regulation of asymmetric cell division by the LIBR-BRD4 axis.

Chen, Hsiao-Fan / Chang, Chia-Ting / Hsu, Kai-Wen / Peng, Pei-Hua / Lai, Joseph Chieh-Yu / Hung, Mien-Chie / Wu, Kou-Juey

Nucleic acids research

2023 Volume 52, Issue 1, Page(s) 154–165

Abstract: Asymmetric cell division (ACD) is a mechanism used by stem cells to maintain the number of progeny. However, the epigenetic mechanisms regulating ACD remain elusive. Here we show that BRD4, a BET domain protein that binds to acetylated histone, is ... ...

Abstract	Asymmetric cell division (ACD) is a mechanism used by stem cells to maintain the number of progeny. However, the epigenetic mechanisms regulating ACD remain elusive. Here we show that BRD4, a BET domain protein that binds to acetylated histone, is segregated in daughter cells together with H3K56Ac and regulates ACD. ITGB1 is regulated by BRD4 to regulate ACD. A long noncoding RNA (lncRNA), LIBR (LncRNA Inhibiting BRD4), decreases the percentage of stem cells going through ACD through interacting with the BRD4 mRNAs. LIBR inhibits the translation of BRD4 through recruiting a translation repressor, RCK, and inhibiting the binding of BRD4 mRNAs to polysomes. These results identify the epigenetic regulatory modules (BRD4, lncRNA LIBR) that regulate ACD. The regulation of ACD by BRD4 suggests the therapeutic limitation of using BRD4 inhibitors to treat cancer due to the ability of these inhibitors to promote symmetric cell division that may lead to tumor progression and treatment resistance.
MeSH term(s)	Asymmetric Cell Division ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Epigenesis, Genetic ; Nuclear Proteins/metabolism ; RNA, Long Noncoding ; Transcription Factors/metabolism ; Cell Division ; Bromodomain Containing Proteins/metabolism
Chemical Substances	Cell Cycle Proteins ; Nuclear Proteins ; RNA, Long Noncoding ; Transcription Factors ; BRD4 protein, human ; Bromodomain Containing Proteins
Language	English
Publishing date	2023-11-20
Publishing country	England
Document type	Journal Article
ZDB-ID	186809-3
ISSN	1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
ISSN (online)	1362-4962 ; 1362-4954
ISSN	0301-5610 ; 0305-1048
DOI	10.1093/nar/gkad1095
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