Abstract
Effect the Mechanism of Emodin Combined with Cp-1 on Proliferation and Apoptosis of Bladder Cancer Cell Line BIU-87
The Biobank of Ningbo First Hospital,1Department of Urology, Ningbo First Hospital, 59 Liuting Street, Ningbo, Zhejiang 315010, China
Correspondence Address:
BIN-BIN YANG, The Biobank of Ningbo First Hospital,1Department of Urology, Ningbo First Hospital, 59 Liuting Street, Ningbo, Zhejiang 315010, China, E-mail: 3556184924@qq.com
To investigate the effect of emodin combined with Cp-1 on the proliferation and apoptosis of bladder cancer cell line BIU-87. BIU-87 cells were randomly divided into control group, Cp-1 group, emodin group, Cp-1 combined with emodin group. Flow cytometry was used to detect the apoptosis of BIU-87 cells. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay was used to detect the proliferation of BIU-87 cells. Western blot and reverse transcription–polymerase chain reaction were used to detect the recepteur d’origine nantais, Caspase-3 and B-cell lymphoma 2 expressions. Compared with control group, the cell survival rate of Cp-1 group, emodin group and Cp-1 combined with emodin groupwas significantly decreased, especially in Cp-1 combined with emodin group, which was significantly lower than that of Cp-1 group and emodin group (p<0.05), while the cell apoptosis rate of Cp-1 group, emodin group and Cp-1 combined with emodin group was significantly increased, especially in Cp-1 combined with emodin group, which was significantly higher than that of Cp-1 group and emodin group (p<0.05) and the expression of recepteur d’origine nantais decreased significantly (p<0.05). Inhibition of recepteur d’origine nantais expression suppressed B-cell lymphoma 2 and increased Caspase-3 significantly (p<0.05). Our results indicated that emodin combined with Cp-1 could enhance the apoptosis and inhibit proliferation of bladder cancer cells. The mechanism may be that emodin can inhibit the expression of recepteur d’origine nantais, down regulated the expression of B-cell lymphoma 2, which increased the expression of caspase-3 in bladder cancer cells and promoted the apoptosis of bladder cancer cells.