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Regulation of MMP-1 and MMP-2 production through CD147/extracellular matrix metalloproteinase inducer interactions

J Sun1, M E Hemler

  • 1Dana Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.

Cancer Research
|March 31, 2001
PubMed

Insights

Extracellular matrix metalloproteinase inducer (EMMPRIN; CD147) homophilic interactions drive tumor cell invasion and MMP production. Inhibiting CD147 may offer a therapeutic strategy against cancer metastasis.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Extracellular matrix metalloproteinase inducer (EMMPRIN; CD147) is a heavily glycosylated protein found on tumor cells.
  • EMMPRIN stimulates matrix metalloproteinase (MMP) production by stromal cells, contributing to tumor progression.

Purpose of the Study:

  • To investigate the role of EMMPRIN (CD147) homophilic interactions in MMP production and tumor cell invasion.
  • To explore the therapeutic potential of targeting CD147 interactions in cancer metastasis.

Main Methods:

  • Utilized CD147 transfectants and immobilized recombinant CD147-Fc fusion protein to study homophilic interactions.
  • Employed anti-CD147 antibody 8G6 and CD147-Fc to inhibit interactions and assess effects on MMP production and cell invasion.
  • Investigated the impact of purified native and deglycosylated CD147 on MMP induction in different cell types.

Main Results:

  • Demonstrated that CD147 engages in homophilic interactions, primarily via its first immunoglobulin domain.
  • Showed that anti-CD147 antibody and CD147-Fc inhibited CD147 homophilic interaction, MMP-2 production by breast cancer cells, and their invasion.
  • Revealed that native CD147 induces MMP-1 and MMP-2 production, suggesting roles in both heterotypic and homotypic interactions, while deglycosylated CD147 antagonized this effect.

Conclusions:

  • Homophilic CD147 interactions are crucial for MMP-2 production and tumor cell invasion.
  • Perturbation of CD147 interactions presents a potential therapeutic strategy for preventing MMP-dependent cancer metastasis.

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