Wnt Signaling in Prostate Cancer Bone Metastases

Abstract

Ace-1-Dkk-1, a canine prostate cancer overexpressing Dkk-1 is used in this study to investigate how enhanced Wnt/JNK signaling could alter metastasis and the bone microenvironment. Evidence was found that Dkk-1 up-regulated the non-canonical Wnt/JNK pathway resulting in downstream alterations in gene expression important in osteoblast stimulation, cell proliferation and epithelial to mesenchymal transformation of tumor cells. Inhibiting non-canonical Wnt/JNK signaling using SP600125, a JNK inhibitor, did not cause the canonical Wnt signaling to resume in Ace-1-Dkk1 cells. However, SP600125 significantly increased the mRNA expression of genes that induce osteoblast differentiation as well as decreased osteolytic genes (decreased RANKL:OPG ratio) in both Ace-1-Dkk1 and Ace-1-Vector cells.

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Document Details

Document Type
Technical Report
Publication Date
Sep 01, 2015
Accession Number
ADA623452

Entities

People

  • Wachiraphan Supsavhad

Organizations

  • Ohio State University

Tags

DTIC Thesaurus Topics

  • Biomedical Research
  • Cancer
  • Cell Line
  • Cells
  • Culture Techniques
  • Department Of Defense
  • Diseases And Disorders
  • Gene Expression
  • Inhibitors
  • Medical Personnel
  • Metastasis
  • Neoplasms
  • Osteoblasts
  • Osteogenesis
  • Prostate
  • Prostate Cancer
  • Students

Fields of Study

  • Biology

Readers

  • Breast cancer cell signaling and growth regulation.
  • Cellular and Molecular Pathways of Apoptosis.
  • Oncology (Cancer Research).