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An Orthotopic Murine Model of Human Prostate Cancer Metastasis
06:48

An Orthotopic Murine Model of Human Prostate Cancer Metastasis

Published on: September 18, 2013

Decreased prostate cancer cell migration by inhibition of the insulin-like growth factor II/Mannose-6-Phosphate

C P Evans1, F Elfman, G Cunha

  • 1Department of Urology, University of California, Davis School of Medicine, Sacramento, CA USA.

Urologic Oncology
|January 14, 2011
PubMed

Insights

The insulin-like growth factor II (IGF-II)/cation-independent mannose-6-phosphate receptor (MPR) is present in prostate cancer cells. Blocking this receptor significantly reduced cancer cell migration, suggesting its role in prostate cancer progression.

Area of Science:

  • Oncology
  • Cell Biology
  • Biochemistry

Background:

  • The insulin-like growth factor II (IGF-II)/cation-independent mannose-6-phosphate receptor (MPR) is a multifunctional receptor involved in endocytosis and intracellular transport.
  • Mannose-6-phosphate (M-6-P) residues on soluble enzymes are recognized by the IGF-II/MPR for transport to lysosomes.

Purpose of the Study:

  • To investigate the expression of IGF-II/MPR in human prostate cancer cells.
  • To determine if IGF-II/MPR mediates prostate cancer cell migration.

Main Methods:

  • Immunoblotting was used to detect intracellular IGF-II/MPR in PC3 prostate cancer cells.
  • Flow cytometry assessed IGF-II/MPR expression on the PC3 cell surface.
  • Scratch migration assays quantified cell motility, with IGF-II/MPR blockade using M-6-P or specific antibodies.

Main Results:

  • IGF-II/MPR was found in the cytoplasm and on the surface of PC3 prostate cancer cells.
  • Blocking IGF-II/MPR with M-6-P or anti-IGF-II/MPR immunoglobulin significantly reduced PC3 cell migration compared to controls.
  • Control treatments with mouse IgG or mannose-1-phosphate did not significantly affect cell migration.

Conclusions:

  • IGF-II/MPR is expressed in human prostate cancer cells (PC3).
  • The findings suggest that IGF-II/MPR plays a significant role in mediating prostate cancer cell motility.
  • Targeting IGF-II/MPR could be a potential therapeutic strategy for prostate cancer.

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