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 invitro. 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.