Expression of VDR and GLi1 in prostate cancer cell line PC-3 and its correlation
10.3969/j.issn.1006-5725.2017.21.008
- VernacularTitle:VDR和GLi1在前列腺癌细胞PC-3中的表达及其相关性
- Author:
Yuandong ZHANG
1
;
Hui ZHAO
;
Jihong SHENG
;
Xiaodong LIU
;
Kangjian LI
;
Runyun GUAN
Author Information
1. 650032,昆明医科大学第一附属医院泌尿外科
- Keywords:
PC-3 cells;
Vitamin D receptor(VDR);
GLi1 protein;
Gene interference
- From:
The Journal of Practical Medicine
2017;33(21):3530-3534
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of lentivirus carrying shRNA-VDR vector on GLi1 in pros-tate cancer PC-3 cells. Methods The cells were cultured according to the culture conditions of PC-3 cells. Expression of VDR and GLi1 in PC-3 cells was detected by fluorescence quantitative PCR and immunocytochemistry SP method.The efficiency of PC-3 cell virus infection was evaluated.The effect of VDR gene interference and GLi1 transcription level on PC-3 cells was detected by RT-PCR.Results Cell culture,cell status was recorded and PC-3 cells were in good condition and the passages was 4 days. Fluorescence quantitative and immunocytochemi-cal SP showed that VDR and GLi1 were expressed in PC-3 cells.The virus infection efficiency showed that the in-fection efficiency was about 95% when adding LV3-NC lentivirus to PC-3 cells at 1:10 ratio. RT-PCR showed that VDR-shRNA lentivirus successfully disturbed VDR expression and decreased by 85%(P < 0.05)compared with the control group after 72 days of VDR-shRNA lentivirus transfection. Transcription level of GLi1 gene in the experimental group increased by 9% compared with the control group(P < 0.05). The transcription level of GLi1 gene in the experimental group increased by 248% compared with the control group(P < 0.05). Conclusion The cultured PC-3 cells were in good condition. VDR and GLi1 genes were expressed in PC-3 cells. Lentivirus showed highest efficiency in infecting PC-3 at 1:10 ratio. When VDR was disturbed,the expression of GLi1 in-creased.In prostate cancer cells,vitamin D can inhibit the Hh signaling pathway and cause GLi1 expression down expression.
