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Related Experiment Videos

Critical function for ADAM9 in mouse prostate cancer.

Lucie Peduto1, Victor E Reuter, David R Shaffer

  • 1Department of Pathology, Memorial Sloan-Kettering Cancer Center, NY 10021, USA.

Cancer Research
|October 19, 2005
PubMed
Summary

Loss of ADAM9 in mouse models reduced prostate tumor aggressiveness and size. ADAM9 (a metalloprotease) may be a viable target for developing new prostate cancer therapies.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • ADAM9, a metalloprotease, is upregulated in various human carcinomas.
  • ADAM9 upregulation is also observed in mouse models of prostate, breast, and intestinal cancers.

Purpose of the Study:

  • To investigate the role of ADAM9 in prostate carcinoma pathogenesis.
  • To evaluate the impact of ADAM9 loss on tumorigenesis in a mouse model.

Main Methods:

  • Utilized W(10) mice, a prostate cancer model, to assess tumorigenesis in the absence of ADAM9.
  • Conducted gain-of-function experiments by overexpressing ADAM9 in mouse prostate epithelium.
  • Performed cell-based assays to explore the molecular mechanisms of ADAM9 action.

Main Results:

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  • Absence of ADAM9 led to well-differentiated tumors in W(10) mice, contrasting with poorly differentiated, larger tumors in controls.
  • ADAM9 overexpression induced epithelial hyperplasia and prostatic intraepithelial neoplasia.
  • ADAM9 was shown to cleave and release epidermal growth factor and FGFR2iiib.

Conclusions:

  • ADAM9 plays a significant role in prostate cancer pathogenesis.
  • ADAM9's contribution to other carcinomas suggests its potential as an antitumor drug target.