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Updated: Aug 14, 2026

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion
09:23

Impedance-based Real-time Measurement of Cancer Cell Migration and Invasion

Published on: April 2, 2020

Tetraspanin KAI1/CD82 suppresses invasion by inhibiting integrin-dependent crosstalk with c-Met receptor and Src

S C Sridhar1, C K Miranti

  • 1Laboratory of Integrin Signaling and Tumorigenesis, Van Andel Research Institute, Grand Rapids, MI 49503, USA.

Oncogene
|December 7, 2005
PubMed

Insights

Loss of CD82 (KAI1) protein suppresses prostate cancer metastasis by inhibiting integrin-mediated cell invasion. CD82 regulates signaling pathways involving c-Met and Src kinases, crucial for cancer cell movement.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • KAI1/CD82, a tetraspanin protein, is recognized as a metastasis suppressor in prostate cancer.
  • The precise mechanisms by which CD82 loss promotes cancer metastasis remain largely unknown.

Purpose of the Study:

  • To elucidate the functional role of CD82 in regulating prostate cancer cell migration and invasion.
  • To investigate the signaling pathways influenced by CD82 expression in prostate cancer.

Main Methods:

  • Utilized the metastatic prostate cancer cell line PC3 with restored CD82 expression.
  • Assessed integrin-mediated cell migration and invasion.
  • Analyzed the activation status of c-Met and Src kinase signaling pathways.
  • Examined the phosphorylation of downstream substrates like p130Cas and FAK Y861.

Main Results:

  • Restoring CD82 expression inhibited integrin-mediated cell migration and invasion without altering integrin levels.
  • CD82 expression significantly reduced integrin-dependent activation of c-Met and Src kinases.
  • Inhibition of c-Met or Src kinase function mimicked the anti-invasive effects of CD82 expression.

Conclusions:

  • CD82 suppresses integrin-induced invasion by negatively regulating signaling pathways involving c-Met and Src kinases.
  • Loss of CD82 may promote prostate cancer metastasis by removing a critical negative regulator of c-Met and Src signaling.

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