Wnt5a signaling is involved in the aggressiveness of prostate cancer and expression of metalloproteinase

Yamamoto, Hideki; Oue, Naohide; Sato, Akira; Hasegawa, Yasuhisa; Matsubara, Akio; Yasui, Wataru; Kikuchi, Akira

doi:10.1038/onc.2009.496

Cited by 197 publications

(211 citation statements)

References 47 publications

(65 reference statements)

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“…These results are also supported by recent studies demonstrating that hydrogen peroxide-mediated proliferation is due to binding of Fra-1/JunD and phospho-c-Jun to the HARP promoter sites (57). JunD was also reported to be involved in migration and invasion of prostate cancer cells by inducing the expression of metalloproteinase-1-mediated by the Wnt5a signaling pathway (72). Interestingly, this action of JunD on prostate cancer cell migration was reported to be opposite to the effect of JunB and c-Jun (73).…”

Section: Figure 6 Tgf-␤1 Did Not Induce Jund or Sapk/jnk Phosphorylasupporting

confidence: 81%

JunD Is Required for Proliferation of Prostate Cancer Cells and Plays a Role in Transforming Growth Factor-β (TGF-β)-induced Inhibition of Cell Proliferation

Millena

Vo²,

Khan

2016

Journal of Biological Chemistry

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Section: Figure 6 Tgf-␤1 Did Not Induce Jund or Sapk/jnk Phosphorylasupporting

confidence: 81%

JunD Is Required for Proliferation of Prostate Cancer Cells and Plays a Role in Transforming Growth Factor-β (TGF-β)-induced Inhibition of Cell Proliferation

Millena

Vo²,

Khan

2016

Journal of Biological Chemistry

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“…The latest induced cytoskeleton reorganization and increased cell motility 82 . In this sense, overexpression of Wnt5a in human prostate cancer cell lines stimulated their invasion activities 83 . Abnormal expression of Wnt5a was also observed in 28% of prostate cancer by immunohistochemistry and positivity was correlated with high Gleason scores and biochemical relapse of prostate cancer.…”

Section: Wnt Signaling Abnormalities In Human Prostate Cancermentioning

confidence: 99%

WNT Signaling in Prostate Development and Carcinogenesis

Kharaishvili¹,

Simkova²,

Makharoblidze³

et al. 2011

BIOMED PAP

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Background. The Wnt signaling pathway is crucial for cell fate decisions, stem cell renewal, regulation of cell proliferation and differentiation. Deregulated Wnt signaling is also implicated in a number of hereditary and degenerative diseases and cancer.Methods and results. This review highlights the role of the Wnt pathway in the regulation of stem/progenitor cell renewal and prostate gland development and how this signaling is altered in prostate cancer. Recent evidence suggests that Wnt signaling regulates androgen activity in prostate cancer cells, enhances androgen receptor expression and promotes the growth of prostate cancer even after androgen ablation therapy. There is also strong evidence that Wnt signaling is enhanced in androgen-ablation resistant tumors and bone metastases.Conclusions. Further study of the modulators of this pathway will be of therapeutic relevance as inhibition of Wnt signaling may have the potential to reduce the self-renewal and aggressive behaviour of prostate cancer while Wnt signaling activation might enhance stem cell activity when tissue regeneration is required.

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“…10,11 The presence of Wnt ligands can enhance the binding of b-catenin to androgen receptor (AR) and promote AR-mediated transcription. 35 Others suggested that IL-6 might modulate the AR nuclear transactivation via STAT3, MAPK, or other signaling cascades. 36,37 In MSCs, activation of phosphorylation of the STAT-3 and MAPK signaling cascades was detected after treatment with either IL-6 or its soluble receptor sIL-6R (Supporting Fig.…”

Section: Discussionmentioning

confidence: 99%

Activation of interleukin-6-induced glycoprotein 130/signal transducer and activator of transcription 3 pathway in mesenchymal stem cells enhances hepatic differentiation, proliferation, and liver regeneration

et al. 2010

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Adult bone marrow-derived mesenchymal stem cells (MSCs) exist in all living species and are capable of differentiating into different types of specific cells. In this study, we demonstrate the therapeutic effectiveness of rat MSC transplantation in D-galactosamine (GalN)-induced acute liver injury and identified the novel pathways which are involved in hepatic differentiation of MSCs. In vivo, intraportal transplantation with 5 Â 10 6 MSCs at 24 hours after GalN administration resulted in significant reduction in serum levels of alanine aminotransferase, aspartate aminotransferase, and total bilirubin compared to the control group. Engrafted MSCs actively proliferated, differentiated, and further enhanced hepatocyte proliferation activity. In vitro, coculture of MSCs with GalN-induced injured hepatocytes showed efficient differentiation and was evidenced by progressive increase in messenger RNA levels of hepatic markers, including albumin, a-fetoprotein, CCAAT-enhancer binding protein a, a-1-antitryspin, and hepatocyte nuclear factor-3b. Immunofluorescent staining revealed that these cells were positive for albumin, a-fetoprotein, and cytokeratin 18, but not clusters of differentiation 34, cytokeratin 19, or OV6. During hepatic differentiation, signal transducer and activator of transcription 3 (STAT3) and mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling were constantly activated, and a gradual down-regulation of b-catenin expression in messenger RNA and protein levels was detected. Hyper-interleukin-6 fusion protein but not interleukin-6 (IL-6) alone caused reduction in b-catenin expression associated with the up-regulation of Wnt-5a in MSCs via activating the glycoprotein 130 (gp130)-mediated STAT3 signaling pathway, which indicates the operation of the trans-signaling mechanism. Activation of IL-6/gp130-mediated STAT3 signaling pathway in MSCs triggered wound healing, cell migration, and proliferation. In conclusion, transplantation of MSCs promotes cell proliferation and organ repair, and activation of IL-6/gp130-mediated STAT3 signaling pathway via soluble IL-6 receptor is crucial in hepatic differentiation of MSCs. Liver Transpl 16:1195-1206. V C 2010 AASLD. Received February 19, 2010 accepted July 7, 2010. Additional Supporting Information may be found in the online version of this article.Abbreviations: AFP, a-fetoprotein; ALT, alanine aminotransferase; APC, adenomatous polyposis coli; AR, androgen receptor; AST, aspartate aminotransferase; CEBP, CCAAT/enhancer binding protein; CK, cytokeratin; CTNN b 1, b-catenin; DAPI, 4 0 ,6-diamidino-2-phenylindole; DVL1, dishevelled; ERK, extracellular signal-regulated kinase; FISH, fluorescent in situ hybridization; FITC, fluorescein isothiocyanate; DMEM, Dulbecco's modified Eagle medium; FBS, fetal bovine serum; GalN, D-galactosamine; GFP, green fluorescent protein; GSK3bglycoprotein synthase kinase 3b; IL, interleukin; IP, immunoprecipitation; MAPK, mitogenactivated protein kinase; mRNA, messenger RNA; MSC, mesenchy...

show abstract

Wnt5a signaling is involved in the aggressiveness of prostate cancer and expression of metalloproteinase

Cited by 197 publications

References 47 publications

JunD Is Required for Proliferation of Prostate Cancer Cells and Plays a Role in Transforming Growth Factor-β (TGF-β)-induced Inhibition of Cell Proliferation

JunD Is Required for Proliferation of Prostate Cancer Cells and Plays a Role in Transforming Growth Factor-β (TGF-β)-induced Inhibition of Cell Proliferation

WNT Signaling in Prostate Development and Carcinogenesis

Activation of interleukin-6-induced glycoprotein 130/signal transducer and activator of transcription 3 pathway in mesenchymal stem cells enhances hepatic differentiation, proliferation, and liver regeneration

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