Suppression of HBXIP Reduces Cell Proliferation, Migration and Invasion In Vitro, and Tumorigenesis In Vivo in Human Urothelial Carcinoma of the Bladder.

Abstract

Hepatitis B X-interacting protein (HBXIP) has been found overexpressed in several types of human cancer, however, the status of HBXIP expression in urothelial carcinoma of the bladder (UCB) has not been explored. In this study, the authors used real-time polymerase chain reaction and Western blot to test the expression of HBXIP in UCB and adjacent tissues. The expression of HBXIP was significantly increased in UCB tissues. In addition, they showed that suppression of HBXIP induced cell cycle arrest and increased cell apoptosis in T24 cells. Also, suppression of HBXIP also decreased T24 and PC3 cell proliferation, migration, and invasion. More importantly, the authors found that inhibition of HBXIP reduced the tumorigenesis in vivo, suggesting that HBXIP plays an important role in UCB progression. These data for the first time showed that HBXIP acts as an oncoprotein in UCB, suggesting that HBXIP may become a potential novel therapeutic target for the treatment of UCB.