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Stable alterations of CD44 isoform expression in prostate cancer cells decrease invasion and growth and alter ligand

Kui Yang1, Yaqiong Tang, Gabriel K Habermehl

  • 1Department of Pathology, University of Colorado Denver Health Science Center, Aurora, Colorado, USA.

BMC Cancer
|January 16, 2010
PubMed
Summary

Re-expressing CD44 standard (CD44s) in prostate cancer (PCa) cells reduced tumor growth and invasion. CD44v7-10 may be a target for improving chemotherapy sensitivity in PCa.

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miRNA Expression Analyses in Prostate Cancer Clinical Tissues
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miRNA Expression Analyses in Prostate Cancer Clinical Tissues

Published on: September 8, 2015

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Dysregulated CD44 expression is common in human cancers, including prostate cancer (PCa).
  • Prostate cancer (PCa) exhibits reduced CD44 standard (CD44s) and increased CD44 variant 7-10 (CD44v7-10) expression.
  • CD44 is a cell surface glycoprotein involved in cell adhesion, migration, and proliferation.

Purpose of the Study:

  • To investigate the functional impact of CD44 standard (CD44s) re-expression and CD44 variant 7-10 (CD44v7-10) knockdown in prostate cancer (PCa) cells.
  • To evaluate the effects on cancer cell invasion, migration, proliferation, adhesion, and chemosensitivity.
  • To assess the potential of CD44 alterations as a gene therapy strategy for PCa.

Main Methods:

  • Utilized retroviral gene delivery to express CD44s (as a fusion or separate protein) or knock down CD44v7-10 in PC-3M PCa cells.
  • Assessed invasion, migration, proliferation, soft agar colony formation, adhesion, and Docetaxel sensitivity.
  • Analyzed xenograft growth and expression of merlin and phospho-merlin via western blot.

Main Results:

  • Re-expression of CD44s, either as a separate or fusion protein, reduced invasion and migration.
  • CD44s re-expression significantly enhanced hyaluronan and osteopontin binding, particularly as a separate protein.
  • CD44v7-10 knockdown sensitized PCa cells to Docetaxel, while CD44s re-expression had minimal effect.
  • CD44s re-expression as a separate protein led to the emergence of hypophosphorylated phospho-merlin.

Conclusions:

  • Stable CD44s re-expression inhibits PCa growth and invasion in vitro, showing potential for gene therapy.
  • Fusion of CD44s to other proteins diminishes its phenotypic effects, especially hyaluronan adhesion.
  • CD44v7-10 may serve as a therapeutic target for enhancing chemosensitization in prostate cancer (PCa).