The Inhibition of Human Telomerase Reverse Transcriptase Expression by Peroxiredoxin I and c-Myc in Prostatic Cancer Cells.
10.4111/kju.2006.47.4.418
- Author:
In Ho CHANG
1
;
Hwa Su KIM
;
Tae Hyung KIM
;
Soon Chul MYOUNG
;
Sang Eun LEE
;
Young Sun KIM
Author Information
1. Department of Urology, Seoul National University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Telomerase reverse transcriptase;
Peroxiredoxin I;
Genes;
myc;
Prostate cancer
- MeSH:
Carcinogenesis;
Cell Line;
DNA, Complementary;
Humans*;
Luciferases;
Peroxiredoxins*;
Plasmids;
Polymerase Chain Reaction;
Prostatic Neoplasms*;
RNA, Messenger;
Telomerase*;
Up-Regulation
- From:Korean Journal of Urology
2006;47(4):418-425
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: We evaluated the hypothesis that the telomerase expression is associated with c-Myc and peroxiredoxin I (Prx I) in patients with prostate cancer. The study determined the link between Prx I, c-Myc and human telomerase reverse transcriptase (hTERT) in prostate cancer cells. MATERIALS AND METHODS: The cDNA of the Prx I gene was obtained by reverse-transcriptase polymerase chain reaction (RT-PCR) amplification. Cotransfections were performed by using a hTERT luciferase reporter plasmid and each expression vector as indicated (c-Myc or Prx I). Empty vectors were used as controls for determining the basal promoter activity. RT-PCR was performed to evaluate the effect of the DEM-induced Prx I mRNA expression. Luciferase assay was performed to evaluate the inhibitory effect of transfected Prx I and the DEM induced Prx I on the transcriptional activity of hTERT in the human prostatic cancer cell lines PC-3 and DU-145. RESULTS: In this study, we found that Prx I could inhibit hTERT expression through direct interaction with c-Myc protein in the prostate cancer cell lines. In addition, it was obvious that Prx I could interact with c-Myc protein. We also found that DEM could induce upregulation of the Prx I mRNA expression and that the increased expression of Prx I could downregulate the expression of hTERT. CONCLUSIONS: Our results demonstrated a direct link between Prx I, c-Myc and hTERT, and we suggest that Prx I regulates cellular immortalization through c-Myc and hTERT, which is activation step in carcinogenesis.
