Upregulated Beta-Arrestin1 Predicts Poor Prognosis And Promotes Metastasis Via Akt/Erk Signaling Pathway In Gastric Cancer

Background: beta-Arrestins have been found to regulate cell proliferation, invasion and migration; transmit antiapoptotic survival signals; and affect other characteristics of tumours. However, their role in gastric cancer (GC) is not clear. We investigated the role and mechanism of beta-arrestins in the regulation of GC.Methods: We first examined beta-arrestins mRNA levels in 17 pairs of GC tissues by qRT-PCR. We also used immunohistochemistry to further examine the expression of beta-arrestins in 60 paraffin-embedded primary GC tissues and 20 normal gastric tissues. Then, the function of beta-arrestin1 was investigated in vitro and in vivo.Results:beta-Arrestin1 was upregulated in GC tissue and was associated with tumour stage, lymph node metastasis, invasion depth and patient sex. High expression of beta-arrestin1 expression predicted poor prognosis in GC. beta-Arrestin1 promoted GC cell proliferation, migration and invasion, and it suppressed E-cadherin expression and upregulated Vimentin expression via AKT/ERK signalling pathway. The in vivo metastasis assays showed that knockdown of beta-arrestin1 reduced lung metastasis and inhibited EMT.Conclusion: The upregulation of beta-arrestin1 predicts poor prognosis and promotes metastasis and epithelial-mesenchymal transition in GC through AKT/ERK signalling pathway. This study may provide therapeutic advances for the treatment and early diagnosis of patients with metastatic GC.