3.Role of Wnt/β-catenin signaling pathway in promoting tumorigenesis of hepatocellular carcinoma.
Lianghai XIE ; Han JIANG ; Fusheng WU
Journal of Southern Medical University 2014;34(6):913-917
Wnt/β-catenin signaling pathway has a close relationship with cancer and is abnormally activated in many human cancers. Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related death worldwide, but the molecular mechanisms of HCC are still poorly understood. Current studies indicate that Wnt/β-catenin signaling pathway plays a key role in the development and progression of HCC. Validating the role and mechanism of Wnt/β-catenin signaling pathway in HCC will provide a theoretical basis for early diagnosis and treatment of HCC. In this review, we summarize the role of Wnt/β-catenin signaling pathway in HCC and the progress of current researches.
Carcinogenesis
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Carcinoma, Hepatocellular
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Humans
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Liver Neoplasms
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Wnt Proteins
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Wnt Signaling Pathway
;
beta Catenin
5.Progress in genetic research on tooth agenesis associated with Wnt/beta-catenin signaling pathway.
Xiujuan ZHU ; Yaping SHEN ; Jing ZHENG
Chinese Journal of Medical Genetics 2021;38(5):506-509
Tooth agenesis is the most common form of congenital craniofacial dysplasia seen in stomatology clinics, which may be caused by genetic and/or environmental factors. Tooth development is regulated by a series of signaling pathways, and variants in any of these strictly balanced signaling cascades can result in tooth agenesis and/or other oral defects. Notably, variants of genes of the Wnt/beta-catenin signaling pathway are important cause for both non-syndromic and syndromic tooth agenesis. This article has provided a review for the molecular genetics of tooth agenesis associated with Wnt/beta-catenin signaling pathway, which may shed lights on the etiology and molecular mechanism of this disease.
Anodontia/genetics*
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Genetic Research
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Humans
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Tooth
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Wnt Proteins/genetics*
;
Wnt Signaling Pathway/genetics*
6.Research Progress on DKK1 Gene in Leukemia.
Feng-Zhi LIU ; Ji-Shi WANG ; Hong-Qian ZHU
Journal of Experimental Hematology 2015;23(4):1190-1193
A number of studies have demonstrated that the methylation of Dickkopf-1 (DKK1) gene promoter is related with the occurrence and development of many neoplastic diseases. By means of binding with corresponding receptors, DKK1 blocks the transduction pathway of Wnt/β-catenin/TCF and inhibits the proliferation and invasion of tumor cells, inducing apoptosis. Leukemia is a hyperplastic disease of hematopoietic stem cell malignant clone. Its pathogenesis has been confirmed to be closely related with the aberrant activation of Wnt signaling pathway. This pathway is associated with the self-renewal and proliferation of the hematopoietic stem cells, which can regulate growth, differentiation, migration of the cells, angiogenesis and embryonic development. Its expression is regulated by some suppressor genes like Dickkopf 1 (DKK1). Leukemia often accompanied by methylation modification of the DKK1 gene, so as to leads to silencing itself and activation of the Wnt signaling pathway, which cause the occurrence of leukemia. Some therapeutic methods on leukemia aiming at DKK1 gene have been reported, among which DKK1 gene was demethylated. The intensive study on the expression and function of DKK1 should be important for the early diagnosis, treatment and prognosis. This article reviews the current progress in this field.
Apoptosis
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Cell Differentiation
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Gene Expression Regulation, Leukemic
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Humans
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Intercellular Signaling Peptides and Proteins
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Leukemia
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Wnt Proteins
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Wnt Signaling Pathway
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beta Catenin
7.Crosstalk between canonical TGF-β/Smad and Wnt/β-catenin signaling pathway.
Cui RAO ; Shan-Li LIN ; Huan WEN ; Hong DENG
Journal of Zhejiang University. Medical sciences 2013;42(5):591-596
TGF-β signaling pathway plays a central role in the signaling networks that control the growth, differentiation of the cell, and the initiation of fibrosis and cancer. Wnt signaling pathway is critical for the embryonic development and the invasion and migration of cancer cells. TGF-β signaling and Wnt signaling, both of which play an important role in regulating embryonic development, fibrotic disease and tumor progression, have a close relationship. Researches find several typical cross points between these two signaling systems, such as Smad, Axin, Dvl and β-catenin. In this review, we focus on the crosstalk between TGF-β signaling and Wnt signaling through these typical factors, intending to better understand the process of fibrosis and tumor progression.
Fibrosis
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metabolism
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Humans
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Neoplasms
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metabolism
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Signal Transduction
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Transforming Growth Factor beta
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physiology
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Wnt Proteins
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physiology
;
Wnt Signaling Pathway
8.The Hairless Gene: A Putative Navigator of Hair Follicle Development.
Jeong Ki KIM ; Bong Kyu KIM ; Jong Keun PARK ; Jee Hyun CHOI ; Sungjoo KIM YOON
Genomics & Informatics 2011;9(3):93-101
The Hairless (HR) gene regulates the expression of several target genes as a transcriptional corepressor of nuclear receptors. The hair follicle (HF), a small independent organ of the skin, resides in the epidermis and undergoes regenerative cycling for normal hair formation. HF development requires many genes and signaling pathways to function properly in time and space, one of them being the HR gene. Various mutations of the HR gene have been reported to cause the hair loss phenotype in rodents and humans. In recent studies, it has been suggested that the HR gene is a critical player in the regulation of the hair cycle and, thus, HF development. Furthermore, the HR gene is associated with the Wnt signaling pathway, which regulates roliferation and differentiation of cells and plays an essential role in hair and skin development. In this review, we summarize the mutations responsible for human hair disorders and discuss the roles of the HR gene in HF development.
Epidermis
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Hair
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Hair Follicle
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Humans
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Phenotype
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Receptors, Cytoplasmic and Nuclear
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Rodentia
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Skin
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Wnt Signaling Pathway
9.Role of the canonical Wnt signaling pathway in heart valve development.
Ran-Ran ZHANG ; Yong-Hao GUI ; Xu WANG
Chinese Journal of Contemporary Pediatrics 2015;17(7):757-762
Formation of the heart valves is one of critical steps in vertebrate cardiac development. Valvular heart anomaly can induce severe cardiac impairment, which is one of most common symptoms for congenital heart defects (CHD). The canonical Wnt/β-catenin signaling pathway, which is essential for numerous developmental processes, has also been suggested to be involved in the regulation of proliferation, differentiation, and migration of myocardium, endocardium and valve primordia at different stages. The canonical Wnt signaling also regulates the endocardial-mesenchymal transformation (EMT) process during the endocardial cushion formation. This paper reviews current knowledge about the canonical Wnt signaling pathway in heart valve development, including the functional diversities of Wnt activity in heart valve development at different stages and its interaction with other valve-relevant signaling pathways and the potential role of canonical Wnt activity in heart valve mesenchymal stem cells at the late developmental stage.
Cell Differentiation
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Cell Proliferation
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Epithelial-Mesenchymal Transition
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Heart Valves
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embryology
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Humans
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Wnt Signaling Pathway
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physiology
10.Ctbp2-mediated β-catenin regulation is required for exit from pluripotency.
Tae Wan KIM ; Sojung KWAK ; Jihoon SHIN ; Byung Hee KANG ; Sang Eun LEE ; Min Young SUH ; Jae Hwan KIM ; In Young HWANG ; Jong Hyuk LEE ; Jinmi CHOI ; Eun Jung CHO ; Hong Duk YOUN
Experimental & Molecular Medicine 2017;49(10):e385-
The canonical Wnt pathway is critical for embryonic stem cell (ESC) pluripotency and aberrant control of β-catenin leads to failure of exit from pluripotency and lineage commitments. Hence, maintaining the appropriate level of β-catenin is important for the decision to commit to the appropriate lineage. However, how β-catenin links to core transcription factors in ESCs remains elusive. C-terminal-binding protein (CtBP) in Drosophila is essential for Wnt-mediated target gene expression. In addition, Ctbp acts as an antagonist of β-catenin/TCF activation in mammals. Recently, Ctbp2, a core Oct4-binding protein in ESCs, has been reported to play a key role in ESC pluripotency. However, the significance of the connection between Ctbp2 and β-catenin with regard to ESC pluripotency remains elusive. Here, we demonstrate that C-terminal-binding protein 2 (Ctbp2) associates with major components of the β-catenin destruction complex and limits the accessibility of β-catenin to core transcription factors in undifferentiated ESCs. Ctbp2 knockdown leads to stabilization of β-catenin, which then interacts with core pluripotency-maintaining factors that are occupied by Ctbp2, leading to incomplete exit from pluripotency. These findings suggest a suppressive function for Ctbp2 in reducing the protein level of β-catenin, along with priming its position on core pluripotency genes to hinder β-catenin deposition, which is central to commitment to the appropriate lineage.
Drosophila
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Embryonic Stem Cells
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Gene Expression
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Mammals
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Transcription Factors
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Wnt Signaling Pathway