Wnt3A activates canonical Wnt signalling in acute lymphoblastic leukaemia (ALL) cells and inhibits the proliferation of B‐ALL cell lines

Nygren, Marit Kveine; Døsen, Guri; Hystad, Marit E.; Stubberud, Heidi; Funderud, Steinar; Rian, Edith

doi:10.1111/j.1365-2141.2006.06442.x

Cited by 51 publications

(41 citation statements)

References 43 publications

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“…Previous studies showed that Wnt3a promoted the proliferation of epidermal stem cells, mesenchymal stem cells, and fibroblast cells, and inhibited the proliferation of B-ALL cell lines (33)(34)(35)(36)(37). As for the melanocyte cell lineage, Dunn et al (16) reported that Wnt3a did not stimulate proliferation of melanoblasts in vitro, and Delmas et al (38) reported that stabilized β-catenin reduced the number of melanoblasts in vivo.…”

Section: Discussionsupporting

confidence: 82%

Wnt3a inhibits proliferation but promotes melanogenesis of melan-a cells

Guo

Yang

Deng

et al. 2012

International Journal of Molecular Medicine

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Abstract. Melanocytes are pigment-producing cells responsible for coloration of skin and hair. Although the importance of Wnt3a in melanocyte development has been well recognized, the role of Wnt3a in mature melanocytes has not been elucidated. This study was conducted to further explore the effects of Wnt3a on melanocyte proliferation and melanogenesis, and to elucidate the possible mechanisms involved. We infected melan-a cells with AdWnt3a to serve as the production source of the Wnt3a protein. MTT assay, 5-bromodeoxyuridine incorporation assay and flow cytometric analysis showed that Wnt3a inhibited the proliferation of melan-a cells and this was associated with decrease of cells in the S phase and increase of cells in the G 1 phase. Melanin content and tyrosinase activity assay revealed that Wnt3a significantly promoted melanogenesis of melan-a cells. Furthermore, western blot analysis showed that Wnt3a upregulated the expression of microphthalmia-associated transcription factor and its downstream target genes, tyrosinase and tyrosinase-related protein 1 in melan-a cells. Collectively, our results suggest that Wnt3a plays an important role in melanocyte homeostasis.

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Section: Discussionsupporting

confidence: 82%

Wnt3a inhibits proliferation but promotes melanogenesis of melan-a cells

Guo

Yang

Deng

et al. 2012

International Journal of Molecular Medicine

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“…21,22 T-cell leukemias tend toward an increase in Wnt1/␤-catenin/lymphoid enhancer factor/T-cell-specific factor (TCF) signaling, and a loss of Wnt5A. 23 However, this is not the case for all T-cell tumors. It has recently been shown that peripheral T lymphomas may be of either T helper cell (Th) 1 or Th2 origin, and although Th1 lymphomas are strongly positive for TCF, a downstream effector of ␤-catenin, those of Th2 origin were, without exception, negative for TCF/lymphoid enhancer factor.…”

Section: Discussionmentioning

confidence: 99%

Activation of Wnt5A signaling is required for CXC chemokine ligand 12–mediated T-cell migration

Ghosh

Collins

Vandanmagsar

et al. 2009

Blood

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“…7,8 In the absence of Wnt ligands, ␤-catenin is targeted by a complex consisting of adenomatous polyposis coli, axin, glycogen synthase kinase-3␤, and casein kinase 1␣ that phosphorylate and mark it for degradation by the ubiquitinproteasome pathway. 9,10 Upon Wnt stimulation, however, the kinase complex is dissociated, and ␤-catenin is not targeted for destruction. The active form of ␤-catenin translocates to the nucleus and, in association with lymphoid enhancer factor (LEF)/Tcell factor (TCF) proteins, activates transcription of target genes like c-Myc, cyclin D1, and Axin2, which are involved in cell proliferation, migration, and survival.…”

Section: Introductionmentioning

confidence: 99%

Aurora kinase A is a target of Wnt/β-catenin involved in multiple myeloma disease progression

Dutta-Simmons¹,

Zhang²,

Görgün

et al. 2009

Blood

100

110

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Multiple myeloma (MM) is a cancer of plasma cells with complex molecular characteristics that evolves from monoclonal gammopathy of undetermined significance, a highly prevalent premalignant condition. MM is the second most frequent hematologic cancer in the United States, and it remains incurable, thereby highlighting the need for new therapeutic approaches, particularly those targeting common molecular pathways involved in disease progression and maintenance, shared across different MM subtypes. Here we report that Wnt/␤-catenin is one such pathway. We document the involvement of ␤-catenin in cell-cycle regulation, proliferation, and invasion contributing to enhanced proliferative and metastatic properties of MM. The pleiotropic effects of ␤-catenin in MM correlate with its transcriptional function, and we demonstrate regulation of a novel target gene, Aurora kinase A, implicating ␤-catenin in G2/M regulation. ␤-catenin and Aurora kinase A are present in most MM but not in normal plasma cells and are expressed in a pattern that parallels progression from monoclonal gammopathy of undetermined significance to MM. Our data provide evidence for a novel functional link between ␤-catenin and Aurora kinase A, underscoring a critical role of these pathways in MM disease progression. (Blood. 2009;114:2699-2708) IntroductionMultiple myeloma (MM) is a neoplasm of plasma cells that infiltrates the bone marrow (BM). Despite recent advances in its treatment, it remains incurable, with a median survival of 6 years. 1 MM accounts for more than 10% of all hematologic malignancies and is the second most frequent hematologic cancer in the United States. It is typically preceded by an age-progressive condition termed monoclonal gammopathy of undetermined significance (MGUS), which is present in 1% to 10% of adults older than 25 years of age and progresses to malignant MM at a rate of 0.5% to 3% annually. 1,2 This disease is characterized by frequent chromosomal aberrations and mutations in several oncogenes and tumor-suppressor genes. 3,4 The Wnt/␤-catenin pathway is significant in cancer development because numerous human malignancies such as colorectal, hepatocellular, and breast cancer harbor activating mutations in critical components of this pathway. 5,6 Normally, the Wnt signaling pathway is active during embryogenesis, hematopoietic stem cell growth, cell differentiation, and tissue development. ␤-catenin, a central effector of the Wnt pathway, is involved in both nuclear and cytoplasmic functions. 7,8 In the absence of Wnt ligands, ␤-catenin is targeted by a complex consisting of adenomatous polyposis coli, axin, glycogen synthase kinase-3␤, and casein kinase 1␣ that phosphorylate and mark it for degradation by the ubiquitinproteasome pathway. 9,10 Upon Wnt stimulation, however, the kinase complex is dissociated, and ␤-catenin is not targeted for destruction. The active form of ␤-catenin translocates to the nucleus and, in association with lymphoid enhancer factor (LEF)/Tcell factor (TCF) proteins, activates transcription...

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Wnt3A activates canonical Wnt signalling in acute lymphoblastic leukaemia (ALL) cells and inhibits the proliferation of B‐ALL cell lines

Cited by 51 publications

References 43 publications

Wnt3a inhibits proliferation but promotes melanogenesis of melan-a cells

Wnt3a inhibits proliferation but promotes melanogenesis of melan-a cells

Activation of Wnt5A signaling is required for CXC chemokine ligand 12–mediated T-cell migration

Aurora kinase A is a target of Wnt/β-catenin involved in multiple myeloma disease progression

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