Effects of Androgen Ablation Therapy in TRAIL Death Ligand and Its Receptors Expression in Advanced Prostate Cancer

KÖKSAL İ. T., ŞANLIOĞLU A. D., Kutlu Ö., ŞANLIOĞLU S.

UROLOGIA INTERNATIONALIS, cilt.84, sa.4, ss.445-451, 2010 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 84 Sayı: 4
  • Basım Tarihi: 2010
  • Doi Numarası: 10.1159/000304510
  • Dergi Adı: UROLOGIA INTERNATIONALIS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.445-451
  • Anahtar Kelimeler: Prostate cancer, TRAIL, Androgen ablation therapy, Hormone-refractory prostate cancer, CELL-LINE LNCAP, INDUCED APOPTOSIS, CARCINOMA-CELLS, FAMILY, SENSITIVITY, COMBINATION, PROGRESSION, SURVIVAL, SIRNA, GENE
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Background: It is not known whether androgen ablation therapy (AAT) influences TRAIL death ligand and its receptors expression of prostate cancer (PCa) cells. Aim: To investigate whether hormonal therapy alters the expression of TRAIL death ligand and TRAIL receptors in patients with advanced PCa. Patients and Methods: 26 untreated and 20 AAT-treated advanced PCa patients were included in the study. The patients who received AAT were divided into two groups based on hormone sensitivity status. TRAIL ligand and receptor expression were determined by a conventional immunohistochemistry method. Results: TRAIL death ligand and TRAIL-R2 death receptor were upregulated in PCa patients who received AAT. Hormone-refractory PCa patients exhibited lower levels of TRAIL death receptor (TRAIL-R1 and TRAIL-R2) expression compared to hormone-sensitive PCa patients. Conclusions: AAT alters TRAIL death ligand and its receptors expression in patients with PCa. Copyright (C) 2010 S. Karger AG, Basel

BACKGROUND: It is not known whether androgen ablation therapy (AAT) influences TRAIL death ligand and its receptors expression of prostate cancer (PCa) cells.

AIM:

To investigate whether hormonal therapy alters the expression of TRAIL death ligand and TRAIL receptors in patients with advanced PCa.

PATIENTS AND METHODS:

26 untreated and 20 AAT-treated advanced PCa patients were included in the study. The patients who received AAT were divided into two groups based on hormone sensitivity status. TRAIL ligand and receptor expression were determined by a conventional immunohistochemistry method.

RESULTS:

TRAIL death ligand and TRAIL-R2 death receptor were upregulated in PCa patients who received AAT. Hormone-refractory PCa patients exhibited lower levels of TRAIL death receptor (TRAIL-R1 and TRAIL-R2) expression compared to hormone-sensitive PCa patients.

CONCLUSIONS:

AAT alters TRAIL death ligand and its receptors expression in patients with PCa.