Effect of AQP9 Expression in Androgen-Independent Prostate Cancer Cell PC3

• Main Authors: Qiwei Chen, Liang Zhu, Bo Zheng, Jinliang Wang, Xishuang Song, Wei Zheng, Lina Wang, Deyong Yang, Jianbo Wang
• Format: Article
• Language: English
• Published: MDPI AG 2016-05-01
• Series: International Journal of Molecular Sciences
• Subjects: prostate cancer; aquaporin 9; RNA interference; proliferation; apoptosis; invasion; ERK signaling pathway
• Online Access: http://www.mdpi.com/1422-0067/17/5/738

It is known that aquaporin 9 (AQP9) in the prostate was strictly upregulated by androgen and may represent a novel therapeutic target for several cancers, but whether AQP9 plays a role in the regulation of androgen-independent prostate cancer still remains unclear. In the present study, AQP9 was determined in prostate cancer and adjacent cancer tissues; AQP9-siRNA was applied to silencing AQP9 in androgen-independent prostate cancer cell PC3 cell line. Western blot and flow cytometry analysis were employed to detect changes in related-function of control and AQP9-siRNA groups. The results showed that AQP9 is significantly induced in cancer tissues than that in adjacent cancer tissues. Moreover, knockdown of AQP9 in PC3 androgen-independent prostate cancer cell prostate cancer cells increased inhibition rates of proliferation. In addition, knockdown of AQP9 resulted in a significant decrease in the expression of the Bcl-2 and with a notable increase in the expression of Bax and cleaved caspase 3, indicated that AQP9 knockdown promoted apoptosis in prostate cancer cells. From wound healing assay and matrigel invasion, we suggested that AQP9 expression affects the motility and invasiveness of prostate cancer cells. Moreover, In order to explore the pathway may be involved in AQP9-mediated motility and invasion of prostate cancer cells, the phosphorylation of ERK1/2 was significant suppressed in AQP9 siRNA-transfected cells compared with that in control cells, suggesting that AQP9 is involved in the activation of the ERK pathway in androgen-independent prostate cancer cells.