Upregulated β-arrestin1 predicts poor prognosis and promotes metastasis via AKT/ERK signaling pathway in gastric cancer

Abstract

Backgroundβ-Arrestins have been found to regulate cell proliferation, invasion and migration; transmit anti-apoptotic 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 β-arrestins in the regulation of GC. MethodsWe first examined β-arrestins mRNA levels in 17 pairs of GC tissues by qRT-PCR. We also used immunohistochemistry to further examine the expression of β-arrestins in 60 paraffin-embedded primary GC tissues and 20 normal gastric tissues. Then, the function of β-arrestin1 was investigated in vitro and in vivo. Resultsβ-Arrestin1 was upregulated in GC tissue and was associated with tumour stage, lymph node metastasis, invasion depth and patient sex. High expression of β-arrestin1 expression predicted poor prognosis in GC. β-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 β-arrestin1 reduced lung metastasis and inhibited EMT. ConclusionThe upregulation of β-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.