Enhanced Wnt/β-catenin and Notch signalling in the activated canine hepatic progenitor cell niche

Schotanus, Baukje A; Kruitwagen, Hedwig S.; Ingh, T.S.G.A.M. van den; Wolferen, Monique E. van; Rothuizen, J.; Penning, Louis C.; Spee, Bart

doi:10.1186/s12917-014-0309-1

Cited by 10 publications

(15 citation statements)

References 56 publications

(60 reference statements)

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“…Our data demonstrate that for canine hepatic organoids, Wnt is important for proliferation and for maintenance of long-term stability, while the inhibition of Wnt enhanced differentiation. This information is interesting in view of the role of Wnt in canine HPCs during liver disease and may partly explain the lack of differentiation during chronic hepatitis or lobular dissecting hepatitis in dogs ( Schotanus et al., 2014 ). It shows that organoid cultures are a useful tool to study stem cell biology and may serve to find potential therapeutic targets to stimulate endogenous adult HPCs to repopulate the liver during diseases.…”

Section: Discussionmentioning

confidence: 99%

Disease Modeling and Gene Therapy of Copper Storage Disease in Canine Hepatic Organoids

et al. 2015

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SummaryThe recent development of 3D-liver stem cell cultures (hepatic organoids) opens up new avenues for gene and/or stem cell therapy to treat liver disease. To test safety and efficacy, a relevant large animal model is essential but not yet established. Because of its shared pathologies and disease pathways, the dog is considered the best model for human liver disease. Here we report the establishment of a long-term canine hepatic organoid culture allowing undifferentiated expansion of progenitor cells that can be differentiated toward functional hepatocytes. We show that cultures can be initiated from fresh and frozen liver tissues using Tru-Cut or fine-needle biopsies. The use of Wnt agonists proved important for canine organoid proliferation and inhibition of differentiation. Finally, we demonstrate that successful gene supplementation in hepatic organoids of COMMD1-deficient dogs restores function and can be an effective means to cure copper storage disease.

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Section: Discussionmentioning

confidence: 99%

Disease Modeling and Gene Therapy of Copper Storage Disease in Canine Hepatic Organoids

et al. 2015

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“…In many cancers, MYC deregulation plays a crucial role in many biological processes, including proliferation, differentiation, apoptosis, and the cell cycle . MYC is also a downstream target of the wnt/β‐catenin, Akt signaling, and Notch signaling pathways, which lead to abnormal proliferation, tumorigenesis, and metastasis. MYC overexpressed in OS has been demonstrated for years .…”

Section: Discussionmentioning

confidence: 99%

A risk signature‐based on metastasis‐associated genes to predict survival of patients with osteosarcoma

Shi

Zhuang

et al. 2020

J of Cellular Biochemistry

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Osteosarcoma (OS) is the most common primary solid malignant bone tumor, and its metastasis is a prominent cause of high mortality in patients. In this study, a prognosis risk signature was constructed based on metastasis-associated genes. Four microarrays datasets with clinical information were downloaded from Gene Expression Omnibus, and 256 metastasis-associated genes were identified by limma package. Further, a protein-protein interaction network was constructed, and survival analysis was performed using data from the Therapeutically Applicable Research to Generate Effective Treatments data matrix, identifying 19 genes correlated with prognosis. Six genes were selected by the least absolute shrinkage and selection operator regression for multivariate cox analysis. Finally, a three-gene (MYC, CPE, and LY86) risk signature was constructed, and datasets GSE21257 and GSE16091 were used to validate the prediction efficiency of the signature. The survival times of low-and highrisk groups were significantly different in the training set and validation set.Additionally, gene set enrichment analysis revealed that the genes in the signature may affect the cell cycle, gap junctions, and interleukin-6 production. Therefore, the three-gene survival risk signature could potentially predict the prognosis of patients with OS. Further, proteins encoded by CPE and LY86 may provide novel insights into the prediction of OS prognosis and therapeutic targets.differentially expressed genes, metastasis, osteosarcoma, risk signature, survival analysis 1 | INTRODUCTION Osteosarcoma (OS), characterized by malignant mesenchymal cells producing an osteoid matrix and fibrillary stroma, is the most common osseous aggressive cancer in children and juveniles and commonly arises at the terminus of the long bones, including distal femurs, proximal tibias, and proximal humor. 1 According to the National Cancer Institute Surveillance, Epidemiology, and End Results program, the frequency of OS has increased by 0.3% per year over the last decade. 2 With the intensification of chemotherapeutic regimens, the 5-year survival rate of OS patients without metastasis has been improved to 60%-70%. 3 By contrast, the survival rate is only 0%-30% in patients with OS with metastasis, 4 indicating that OS metastasis is associated poor longterm prognosis. However, metastasis-associated molecules Yi Shi and Ronghan He contributed equally to this work.

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“…In previous studies, c-MYC has been characterized as an oncogene that is correlated with cell proliferation, 31 differentiation 32 and metastasis. 33 C-Myc is a downstream targeted protein in many types of proliferation and metastasis linked signaling pathways, such as the Wnt pathway, 13 Akt signaling 34 and Notch signaling. 14 In human non-small-cell lung carcinoma, the overexpression of c-Myc enhances tumor growth.…”

Section: Discussionmentioning

confidence: 99%

“…In Wnt/ beta-catenin signaling, c-Myc is targeted by beta-catenin, which leads to abnormal proliferation and tumorigenesis. 13 In the Notch pathway, c-MYC targeting by NOTCH1 induces a series of transcriptional pathways promoting leukemic cell growth. 14 As a key of oncogene, c-MYC has been reported in many types of cancers, such as lung cancer, 15 breast cancer 16 and liver cancer.…”

Section: Introductionmentioning

confidence: 99%

Nucleoside diphosphate kinase B promotes osteosarcoma proliferation through c-Myc

Yuan

et al. 2018

Cancer Biology & Therapy

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Osteosarcoma (OS) is one of the most common primary bone tumors and has a high disablity rate and case-fatality rate. The protracted stagnancy of the chemotherapy program and surgical technology for OS treatment prompted us to focus on the mechanisms of cancer carcinogenesis progression in OS. Nucleoside diphosphate kinase B (NME2) is a type of nucleoside diphosphate kinase that plays an important role in cellular processes. In this study, we report overexpression of NME2 in OS cell lines and correlate this overexpression with the clinicopathologic features of osteosarcoma. We used si-NME2 to downregulate expression of NME2 in OS cell lines. The results of the CCK8 and clone forming assays show that NME2 promotes OS cell line proliferation. Western blot assays show that deregulation of NME2 results in enhanced the expression of c-Myc, which promotes OS proliferation.

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Enhanced Wnt/β-catenin and Notch signalling in the activated canine hepatic progenitor cell niche

Cited by 10 publications

References 56 publications

Disease Modeling and Gene Therapy of Copper Storage Disease in Canine Hepatic Organoids

Disease Modeling and Gene Therapy of Copper Storage Disease in Canine Hepatic Organoids

A risk signature‐based on metastasis‐associated genes to predict survival of patients with osteosarcoma

Nucleoside diphosphate kinase B promotes osteosarcoma proliferation through c-Myc

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