Abstract
BackgroundHuman androgen receptor (AR) functions as a steroid-hormone activated transcription factor. The receptor binds to its ligand (testosterone or dihydrotestosterone) and is translocated to the nucleus to stimulate the transcription of androgen responsive genes. Mutations in the ligand binding domain (LBD) impair the receptor activity and play a crucial role in the development and progression of prostate cancer (PCa). Materials and methodsThis work was designated to investigate the restriction integrity of the LBD and its association with benign prostatic hyperplasia (BPH) and prostate cancer. Exons of this domain (exons: 4–8) were amplified from prostate tissue of BPH and PCa patients and the restriction polymorphism was investigated by SmlI, HphI and Tsp45I restriction enzymes in both BPH and PCa groups. ResultsData revealed the integrity of exons 4–6 in both BPH and PCa patients. Exons 7 and 8, however have kept their constitutional pattern only in BPH patients. Hph1 site showed an abnormal restriction pattern in 40% and 26.7% of PCa patients. Also, Tsp45I demonstrated restriction polymorphism in 20% and 13% of PCa patients. ConclusionOur results indicate that the loss of the restriction integrity in the C-terminal part (exons: 7 and 8) of the LBD is associated with the progression of benign prostatic hyperplasia to prostate cancer.
Highlights
Peer review under responsibility of Ain Shams University.Prostate cancer is the sixth leading cause of cancer-related deaths among men [1]
Our results indicate that the loss of the restriction integrity in the C-terminal part of the ligand binding domain (LBD) is associated with the progression of benign prostatic hyperplasia to prostate cancer
To investigate the integrity of the restriction pattern of LBD and its possible association with the progression from benign to invasive prostate cancer, we investigated the frequency of LBD polymorphisms, using SmlI, HphI and Tsp45I restriction enzymes in both premalignant and malignant tissues compared to the wild type restriction pattern identified by the Restriction-Mapper
Summary
Peer review under responsibility of Ain Shams University.Prostate cancer is the sixth leading cause of cancer-related deaths among men [1]. Peer review under responsibility of Ain Shams University. Prostate cancer cells usually acquire a large number of genetic alterations including point mutations, deletions, amplifications and translocations. Production and hosting by Elsevier B.V. on behalf of Ain Shams University. Human androgen receptor (AR) functions as a steroid-hormone activated transcription factor. The receptor binds to its ligand (testosterone or dihydrotestosterone) and is translocated to the nucleus to stimulate the transcription of androgen responsive genes. Mutations in the ligand binding domain (LBD) impair the receptor activity and play a crucial role in the development and progression of prostate cancer (PCa)
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