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[Molecular targeted therapy for prostate cancer]

Yoshihiro Hashimoto1, Hiromichi Naruyama, Ryousuke Ando

  • 1Department of Urology, Nagoya City University Medical Association.

Hinyokika Kiyo. Acta Urologica Japonica
|February 12, 2008
PubMed

Insights

Understanding prostate cancer progression and anti-androgen therapy resistance is crucial. This review explores cell cycle regulators and coactivators like SRC-3, highlighting their roles in prostate cancer growth and survival.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Context:

  • Prostate cancer growth is androgen-dependent.
  • Resistance to anti-androgen therapy is a significant clinical challenge.
  • The molecular mechanisms driving therapy resistance are not fully understood.

Purpose:

  • To review the roles of cell cycle regulators and steroid receptor coactivators in prostate cancer.
  • To elucidate the molecular mechanisms underlying resistance to anti-androgen therapy.

Summary:

  • Cyclin E enhances androgen receptor activity and prostate cancer cell proliferation.
  • p27 can reduce prostate cancer xenograft tumor size.
  • Steroid receptor coactivator-3 (SRC-3) overexpression modulates AKT signaling, promoting prostate cancer cell growth, while its down-regulation suppresses growth.

Impact:

  • Findings provide insights into molecular targets for prostate cancer treatment.
  • Understanding these pathways may help overcome anti-androgen therapy resistance.
  • Highlights the potential of targeting SRC-3 and cell cycle regulators in prostate cancer therapy.

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