MDA-9/syntenin is essential for factor VIIa-induced signaling, migration, and metastasis in melanoma cells

J Biol Chem. 2015 Feb 6;290(6):3333-48. doi: 10.1074/jbc.M114.606913. Epub 2014 Dec 10.

Abstract

Melanoma differentiation associated gene-9 (MDA-9), also known as syntenin, is a novel gene that positively regulates cancer cell motility, invasion, and metastasis through distinct biochemical and signaling pathways, but how MDA-9/syntenin is regulated in response to signals with the extracellular environment and promotes tumor progression is unclear. We now demonstrate that MDA-9/syntenin is dramatically up-regulated by a combination of rFVIIa and factor F(X) in malignant melanoma. Induction of MDA-9/syntenin in melanoma was found to occur in a thrombin-independent signaling pathway and involves the PAR-1/c-Src/Rho GTPases Rac1 and Cdc42/c-Jun N-terminal kinase axis resulting in the activation of paxillin, NF-κB, and matrix metalloproteinase-2 (MMP-2). MDA-9/syntenin physically interacts with c-Src through its PDZ binding motif following stimulation of melanoma cells with rFVIIa and FX. We also document that induction of this signaling pathway is required for TF·FVIIa·Xa-induced cell migration, invasion, and metastasis by melanoma cells. The present finding uncovers a novel role of MDA-9/syntenin as an important TF·FVIIa·Xa/PAR-1-regulated gene that initiates a signaling circuit essential for cell motility and invasion of metastatic melanoma. In these contexts, targeting TF·FVIIa·Xa and its relevant downstream targets such as MDA-9/syntenin, may represent a novel therapeutic strategy to control the evolution of neoplastic cells.

Keywords: Adaptor Protein; Cell Invasion; Cell Migration; Melanoma; PDZ Domain; Tissue Factor.

Publication types

  • Research Support, Non-U.S. Gov't
  • Retracted Publication

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cell Movement*
  • Factor VIIa / metabolism*
  • Factor X / metabolism
  • Gene Expression Regulation, Neoplastic
  • Humans
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • Matrix Metalloproteinase 2 / metabolism
  • Melanoma / metabolism*
  • Melanoma / pathology
  • Mice
  • NF-kappa B / metabolism
  • NIH 3T3 Cells
  • Neoplasm Metastasis
  • PDZ Domains
  • Paxillin / metabolism
  • Protein Binding
  • Receptor, PAR-1 / metabolism
  • Signal Transduction*
  • Syntenins / chemistry
  • Syntenins / genetics
  • Syntenins / metabolism*
  • Up-Regulation
  • cdc42 GTP-Binding Protein / metabolism
  • rac1 GTP-Binding Protein / metabolism
  • src-Family Kinases / metabolism

Substances

  • NF-kappa B
  • Paxillin
  • Receptor, PAR-1
  • SDCBP protein, human
  • Syntenins
  • Factor X
  • src-Family Kinases
  • JNK Mitogen-Activated Protein Kinases
  • Factor VIIa
  • MMP2 protein, human
  • Matrix Metalloproteinase 2
  • cdc42 GTP-Binding Protein
  • rac1 GTP-Binding Protein