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The Inhibition of Human Telomerase Reverse Transcriptase Expression by Peroxiredoxin I and c-Myc in Prostatic Cancer Cells
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ÀåÀÎÈ£ ( Chang In-Ho )
¼¿ï´ëÇб³ ÀÇ°ú´ëÇÐ ºñ´¢±â°úÇб³½Ç
±èȼö ( Kim Hwa-Su )
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±èÅÂÇü ( Kim Tae-Hyoung )
Áß¾Ó´ëÇб³ ÀÇ°ú´ëÇÐ ºñ´¢±â°úÇб³½Ç
¸í¼øö ( Myung Soon-Chul )
Áß¾Ó´ëÇб³ ÀÇ°ú´ëÇÐ ºñ´¢±â°úÇб³½Ç
ÀÌ»óÀº ( Lee Sang-Eun )
¼¿ï´ëÇб³ ÀÇ°ú´ëÇÐ ºñ´¢±â°úÇб³½Ç
±è¿µ¼± ( Kim Young-Sun )
Áß¾Ó´ëÇб³ ÀÇ°ú´ëÇÐ ºñ´¢±â°úÇб³½Ç
KMID : 0358320060470040418
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. (Korean J Urol 2006;47:418-425)
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Telomerase reverse transcriptase; Peroxiredoxin I; Genes; myc; Prostate cancer
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