Abstract

Caffeic acid phenethyl ester (CAPE) treatment suppressed proliferation, colony formation, and cell cycle progression in PC-3 human prostate cancer cells. CAPE decreased protein expression of cyclin D1, cyclin E, SKP2, c-Myc, Akt1, Akt2, Akt3, total Akt, mTOR, Bcl-2, Rb, as well as phosphorylation of Rb, ERK1/2, Akt, mTOR, GSK3α, GSK3β, PDK1; but increased protein expression of KLF6 and p21Cip1. Microarray analysis indicated that pathways involved in cellular movement, cell death, proliferation, and cell cycle were affected by CAPE. Co-treatment of CAPE with chemotherapeutic drugs vinblastine, paclitaxol, and estramustine indicated synergistic suppression effect. CAPE administration may serve as a potential adjuvant therapy for prostate cancer.

Highlights

  • Prostate cancer is one of the most common non-cutaneous carcinoma of men in western countries

  • Trypan blue staining indicated that Caffeic acid phenethyl ester (CAPE) dose-dependently inhibited proliferation of PC-3 cells with an EC50 around 20.4 mM (Fig. 1A)

  • Colony formation assay revealed that treatment of 10 mM and 20 mM CAPE efficiently inhibited the formation of PC-3 colonies in soft agar (Fig. 1C)

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Summary

Introduction

Prostate cancer is one of the most common non-cutaneous carcinoma of men in western countries. More than 80% of patients died from prostate cancer developed bone metastases [1,2,3]. In 1941, Charles Huggins discovered that deprivation of androgen caused regression of hormone-responsive metastatic prostate cancer [4]. Androgen ablation therapy has become the primary treatment for metastatic prostate cancer. Most prostate cancer patients receiving androgen ablation therapy develop recurrent, castration-resistant tumors within 12–33 months after treatment. The median overall survival time is 1–2 years after tumor relapse [5,6]. Chemotherapy is usually applied for treatment of metastatic hormone-refractory prostate cancer [7]

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