Bone-targeted Src SH2 inhibitors block Src cellular activity and osteoclast-mediated resorption

Bone. 2001 Jan;28(1):54-64. doi: 10.1016/s8756-3282(00)00427-0.

Abstract

Src, a nonreceptor tyrosine kinase, is an important regulator of osteoclast-mediated resorption. We have investigated whether compounds that bind to the Src SH2 domain inhibit Src activity in cells and decrease osteoclast-mediated resorption. Compounds were examined for binding to the Src SH2 domain in vitro using a fluorescence polarization binding assay. Experiments were carried out with compounds demonstrating in vitro binding activity (nmol/L range) to determine if they inhibit Src SH2 binding and Src function in cells, demonstrate blockade of Src signaling, and lack cellular toxicity. Cell-based assays included: (1) a mammalian two-hybrid assay; (2) morphological reversion and growth inhibition of cSrcY527F-transformed cells; and (3) inhibition of cortactin phosphorylation in csk-/- cells. The Src SH2 binding compounds inhibit Src activity in all three of these mechanism-based assays. The compounds described were synthesized to contain nonhydrolyzable phosphotyrosine mimics that bind to bone. These compounds were further tested and found to inhibit rabbit osteoclast-mediated resorption of dentine. These results indicate that compounds that bind to the Src SH2 domain can inhibit Src activity in cells and inhibit osteoclast-mediated resorption.

MeSH terms

  • Actins / metabolism
  • Amino Acid Sequence
  • Animals
  • Bone Resorption / metabolism*
  • Cell Line, Transformed
  • Dentin / metabolism
  • Diphosphonates / chemistry
  • Diphosphonates / metabolism*
  • Diphosphonates / pharmacology
  • Enzyme Inhibitors / chemistry
  • Enzyme Inhibitors / metabolism
  • Enzyme Inhibitors / pharmacology
  • Fibroblasts / cytology
  • Humans
  • Ligands
  • Mammals
  • Mice
  • Molecular Sequence Data
  • Osteoclasts / cytology
  • Osteoclasts / metabolism*
  • Osteoporosis / metabolism
  • Rabbits
  • Radioligand Assay
  • Rats
  • Tritium
  • Two-Hybrid System Techniques
  • src Homology Domains / physiology*
  • src-Family Kinases / antagonists & inhibitors
  • src-Family Kinases / metabolism*

Substances

  • AP21946
  • AP22188
  • AP22408
  • AP22409
  • Actins
  • Diphosphonates
  • Enzyme Inhibitors
  • Ligands
  • Tritium
  • src-Family Kinases