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AQP5

Aquaporin 5 (AQP5), a transmembrane protein, is known for its involvement in the progress of many diseases such as chronic kidney disease and systemic disease. Recently, AQP5 has been reported to play an important role in cancer progression. However, little is known about its precise functions in hepatocellular carcinoma (HCC). This study aimed to investigate the specific role of AQP5 in HCC. The results showed that AQP5 was highly expressed in HCC cell lines and its down-regulation inhibited HCC cell invasion and tumor metastasis in vitro and in vivo. In addition, down-regulation of AQP5 suppressed the epithelial-mesenchymal transition (EMT) process in HCC cells by modulating EMT-related molecules such as E-cadherin, alpha-catenin, N-cadherin and Vimentin. Further studies on corresponding mechanisms indicated that AQP5 down-regulation inhibited HCC metastasis and EMT partly via inactivation of the NF-kappaB signaling pathway. Taken together, these findings suggest that AQP5 may be a potential therapeutic target for HCC.CI - Copyright (c) 2017 Elsevier Inc. All rights reserved.

epithelial-mesenchymal transition (EMT) has emerged as an important determinant role in colorectal cancer (CRC) metastasis. It has been reported that aquaporin 5 (AQP5) is closely linked to CRC metastasis. However, the effect of AQP5 on the EMT process of CRC remains unknown. The current study showed that overexpression of AQP5 activated EMT in CRC cells. Cairicoside E (CE), a natural resin glycoside compound isolated from Ipomoea cairica, showed promising cytotoxic activity in our previous report. Further investigation found that CE inhibited the expression of AQP5 and the EMT process. Moreover, the inhibitory effect of CE on EMT was reversed by overexpression of AQP5. Importantly, CE also suppressed the EMT and p-Smad2/3 induced by TGF-beta1. On the other hand, overexpression of AQP5 up-regulated the p-Smad2/3, which resulted in the activation of EMT. After silencing of AQP5, CE had no significant effect on EMT markers and p-Smad2/3 induced by TGF-beta1, indicating that CE inhibited the EMT through down-regulation of AQP5 and suppression of p-Smad2/3. CE also inhibited the AQP5 expression in the lung metastatic nodules of HCT-116 cells in vivo. Our findings suggested that CE may serve as a promising drug for the treatment of CRC metastasis.CI - (c) 2017 Wiley Periodicals, Inc.