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Intermediate-conductance-Ca2+activated K+channels are involved in regulating cell cycle of endometrial cancer cells / 第二军医大学学报
Article in Chinese | WPRIM (Western Pacific) | ID: wpr-839994
Responsible library: WPRO
ABSTRACT
Objective To study the expression of intermediate? conductance? Ca2+-activatedK+ (KCa3.1) channelsin Endometrial cancer tissues and their role in regulating cell cycle of endometrial cancer cells.Methods Real?time PCR and Western blotting analysis were used to examine the expression of KCa3.1 channels in 25 normal endometrial specimens,26 atypical hyperplasia specimens and 25 endometrial cancer specimens.Clotrimazole (an inhibitor of KCa3.1 channel)and RNA interference (RNAi) targeting KCa3.1 channel were used to block KCa3.1, so as to explore the role of KCa3.1 channels in regulating the cell cycle of endometrial cancercells.Results The expression levels of KCa3.1 mRNA and protein in endometrial carcinoma were significantly higher than those in the typical hyperplasia endometrial and normal endometrial tissues (P<0.01).Clotrimazole retarded cell cycle at G0-G1 phase in a dose-dependent manner and reduced HEC-1-Acells of S phase.KCa3.1 protein level in cells transfected with target-KCa3.1 siRNA was only (40.27±6.09)%that of cells transfected with negative control.Transfection with target?KCa3.1 siRNA also retarded cell cycle of HEC-1A cells atG0-G1phase,and reduced cells of S phase compared with negative control siRNA. Meanwhile,transfection with target=-KCa3.1 siRNA also reduced cyclinD1 protein expression in HEC-1A cells. Conclusion The expressions of KCa3.1 channels are elevated in endometrial cancer tissues,and KCa3.1 channels may influence cell cycle through regulating cyclinD1.

Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Academic Journal of Second Military Medical University Year: 2011 Document type: Article
Full text: Available Database: WPRIM (Western Pacific) Language: Chinese Journal: Academic Journal of Second Military Medical University Year: 2011 Document type: Article
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