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

第一作者： Xu, Tingjuan

作者： Xu, Tingjuan;Shen, Guodong;Cheng, Min;Wu, Xinchun;Hu, Shilian;Xu, Tingjuan;Shen, Guodong;Cheng, Min;Wu, Xinchun;Hu, Shilian;Xu, Yayuan

作者机构：

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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