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ADAM10 as a therapeutic target for cancer and inflammation

Howard C Crawford1, Peter J Dempsey, Gordon Brown

  • 1Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY 11794, USA.

Current Pharmaceutical Design
|July 16, 2009
PubMed

Insights

ADAM10, an enzyme, cleaves substrates to activate pathways in cancer and inflammation. Inhibiting ADAM10 may offer new therapeutic strategies for these diseases.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cell Biology

Background:

  • Cancer and chronic inflammatory diseases involve dysregulated signal transduction pathways.
  • Extracellular metalloproteinases, like ADAM10, mediate key steps in activating these pathways through substrate cleavage.
  • ADAM10 plays a role in both shedding of membrane-bound proteins and regulated intramembrane proteolysis (RIP).

Purpose of the Study:

  • To discuss the established functions of ADAM10.
  • To explore the implications of ADAM10 inhibition in disease progression.
  • To highlight ADAM10 as a potential drug target for cancer and inflammatory diseases.

Main Methods:

  • Literature review of ADAM10 functions and substrate interactions.
  • Analysis of ADAM10's role in cancer and inflammatory disease pathogenesis.
  • Discussion of the therapeutic potential of targeting ADAM10.

Main Results:

  • ADAM10 is implicated in the shedding and RIP of numerous substrates, including Notch, E-cadherin, EGF, ErbB2, and inflammatory cytokines.
  • Dysregulation of ADAM10 activity contributes to cancer progression and inflammatory diseases.
  • ADAM10 is a significant factor in the pathologies of these diseases.

Conclusions:

  • ADAM10's critical role in activating signaling pathways makes it a promising drug target.
  • Understanding ADAM10's functions is crucial for developing novel treatments for cancer and inflammatory conditions.
  • Inhibition of ADAM10 presents a potential therapeutic avenue for diseases driven by its activity.

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