β-arrestin2 promotes 5-FU-induced apoptosis via the NF-κB pathway in colorectal cancer

Abstract

It has been demonstrated that β-arrestin2 is involved in the initiation and development of many types of cancers. However, its role in colorectal cancer (CRC) remains poorly understood. The present study investigated the role of β-arrestin2 in CRC using CRC patient tissues as well as the LoVo and HCT116 CRC cell lines. Briefly, significantly higher expression of β-arrestin2 was observed in CRC tissues compared with normal colon tissues. In addition, the downregulation of β-arrestin2 reduced 5-FU-induced apoptosis in the LoVo cells, while the overexpression of β-arrestin2 increased the apoptosis of HCT116 cells in vitro. Furthermore, the downregulation of β-arrestin2 reduced the expression of the pro-apoptotic proteins cleaved-caspase-3 and Bax, and increased the expression of the anti-apoptotic protein Bcl-2 after 5-FU treatment. In addition, the expression of p-p65 was increased after the β-arrestin2 downregulation and was decreased after the β-arrestin2 overexpression. However, β-arrestin2 downregulation had no effect on the proliferation, migration and invasion capacity of the LoVo cells. In conclusion, these results indicated that β-arrestin2 promoted 5-FU-induced CRC cell apoptosis via the NF-κB pathway and may be used as a prognosis marker for CRC.