Abstract

Peroxisome proliferator-activated receptor- (PPAR)- is a ligand-activated transcriptional factor belonging to steroid receptor superfamily. PPAR- plays a role in both adipocyte differentiation and tumorigenesis. Up to date, PPAR- is expressed in various cancer tissues, and PPAR- ligand induces growth arrest of these cancer cells. In this study, we examined the expression of PPAR- in prostate cancer (PC) and testicular cancer (TC) by RT-PCR and immunohistochemistry, and we also examined the effect of PPAR- ligand in these cells by MTT assay, hoechest staining, and flow cytometry. PPAR- expression was significantly more extensive and intense in malignant tissues than in normal tissues. PPAR- ligand induced the reduction of malignant cell viability through apoptosis. These results demonstrated that the generated PPAR- in PC and TC cells might play an important role in the tumorigenesis. PPAR- may become a new target in the treatment of PC and TC.

Highlights

  • Prostate cancer (PC) comprises 32% of all cancers in American men and is on the increase worldwide

  • To evaluate whether or not cell death induced by Peroxisome proliferator-activated receptor-γ (PPAR)-γ ligands was through apoptosis, we evaluated the chromatin morphology of PC (PC3) cell and testicular cancer (TC) cell (NEC-8) lines using hoechst staining

  • PPAR-α is highly expressed in the liver, heart, kidney, muscle, brown adipose tissue, and gut, which exhibit high carbolic rates of fatty acid

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Summary

Introduction

Prostate cancer (PC) comprises 32% of all cancers in American men and is on the increase worldwide. PC is frequently diagnosed at a clinically localized stage, making it amenable to the therapy. It remains the second most common cause of cancer death in men. These patients generally respond to androgen deprivation therapy, but the vast majority eventually experience disease progression and become refractory to sustained hormonal manipulation. Such patients progress with a rise in their serum prostate-specific antigen level. Standard therapeutic options at this stage of disease are limited, and while there has been some success with chemotherapy for hormone-refractory prostate cancer patients, the response is generally short lived [1]

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