Upregulated beta-arrestin1 predicts poor prognosis and promotes metastasis via AKT/ERK signaling pathway in gastric cancer
文献类型: 外文期刊
作者: Xu, Tingjuan 1 ; Shen, Guodong 1 ; Cheng, Min 1 ; Wu, Xinchun 1 ; Xu, Yayuan 3 ; Hu, Shilian 1 ;
作者机构: 1.Univ Sci & Technol China, Inst Gerontol, Affiliated Hosp USTC 1, Div Life Sci & Med, Lujiang Rd 17, Hefei 230001, Anhui, Peoples R China
2.Anhui Prov Key Lab Tumor Immunotherapy & Nutr The, Hefei 230001, Anhui, Peoples R China
3.Anhui Acad Agr Sci, Agroprod Proc Res Inst, Hefei 230031, Anhui, Peoples R China
关键词: Gastric cancer; beta-arrestin1; Prognosis; Metastasis; Epithelial-mesenchymal transition
期刊名称:PATHOLOGY RESEARCH AND PRACTICE ( 影响因子:3.25; 五年影响因子:2.74 )
ISSN: 0344-0338
年卷期: 2020 年 216 卷 12 期
页码:
收录情况: SCI
摘要: 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.
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