Affiliation:
1. Department of Biology, Sanandaj Branch Islamic Azad University Sanandaj Iran
2. Department of Anesthesiology, Pharmacology and Therapeutics The University of British Columbia Vancouver British Columbia Canada
3. Department of Clinical Biochemistry Ilam University of Medical Sciences Ilam Iran
Abstract
AbstractBackgroundThe androgen receptor (AR) has been studied as an approach to cancer therapy.AimsWe used human breast cancer‐derived cells with high, low, and very low expression levels of AR, in addition to prostate cancer‐derived LNCaP and DU‐145 cells as a positive and negative controls to examine apoptosis caused by a synthetic peptide that targets ARs.Methods and ResultsThe peptide was produced to inhibit AR transactivation in breast cancer cell lines. We then measured cell viability, caspase‐3 activity, and the ratio of Bax/Bcl‐2. The findings indicated that the peptide (100–500 nM) in the presence of dihydrotestosterone (DHT) reduced cell growth in cells with high and low expression level of AR (p < .001), but not in cells with very low levels of AR. Treatment with 100–500 nM of peptide activated caspase‐3 and increased the ratio of Bax/Bcl‐2 in cells with high and low expression levels of AR. Also, increasing concentrations of the peptide (100–500 nM) reduced BrdU incorporation in the presence of DHT and promoted apoptosis in cells with high and low expression levels of AR (p < .001).ConclusionThe findings indicate the peptide significantly increased apoptosis in cancer cells.