Alterations in Calcium-Activated Potassium Channel Expressions in Human Prostate Cancer.
10.4111/kju.2006.47.5.548
- Author:
Duk Yoon KIM
1
;
Eun Kyoung YANG
;
Jung Wook KIM
Author Information
1. Department of Urology, Catholic University of Daegu School of Medicine, Korea. dykim@mail.cu.ac.kr
- Publication Type:Original Article
- Keywords:
Prostate cancer;
Large-conductance calcium-activated potassium channels;
Small-conductance calcium-activated potassium channels
- MeSH:
Cell Line;
Connexins;
Humans*;
Large-Conductance Calcium-Activated Potassium Channels;
Nitrogen;
Polymerase Chain Reaction;
Potassium;
Potassium Channels, Calcium-Activated*;
Prostate*;
Prostatectomy;
Prostatic Hyperplasia;
Prostatic Neoplasms*;
RNA;
RNA, Messenger;
Small-Conductance Calcium-Activated Potassium Channels;
Sodium Channels
- From:Korean Journal of Urology
2006;47(5):548-552
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Recent studies have shown that potassium (K+) and sodium channels are involved in prostate cell growth. However, a great many of the studies have been done in prostate cancer cell lines and there are only scant studies on prostate cancer and benign prostatic hypertrophy (BPH) tissue. The present study was aimed to evaluate the alterations of the calcium-activated K+ channel (KCa) expression in prostate cancer, and to compare them with the expression profiles in human BPH tissue to understand their potential role in the progression of prostate cancer. MATERIALS AND METHODS: The prostate tissues obtained from radical prostatectomy (n=10) and transurethral resection of the prostate (n=18) were quickly frozen in liquid nitrogen for the RNA measurements. The protein and mRNA levels of the KCa subtypes and connexins were measured by performing immunoblot analysis and reverse-transcription polymerase chain reaction, respectively. RESULTS: The mRNA levels of type 2 (SK2) and type 3 (SK3) small-conductance and large-conductance (BK) KCas in the prostate cancer tissues were decreased more than 50% compared with those in the BPH samples. In addition, the BK and SK2 protein levels in prostate cancer were also significantly lower than those in the BPH. As reported previously, the connexin 26 and 43 transcript signals in the prostate cancer were significantly reduced compared with those in the BPH samples. CONCLUSIONS: These results suggest that the impaired expression of KCas may have a role in tumor progression via aberrant and uncontrolled prostate cell growth.
