OncoTargets and Therapy (Mar 2020)
The Role of β-Arrestin1 in Esophageal Squamous Cell Carcinoma
Abstract
Zhijie Tan, 1 Bin Li, 2 Xia Dong, 3 Wenxing Liu, 4 Shanshan Liu 1 1Department of Gastroenterology, People’s Hospital of Central District of Jinan, Shandong 250022, People’s Republic of China; 2Department of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Shandong 250021, People’s Republic of China; 3Department of Anesthesiology, People’s Hospital of Central District of Jinan, Shandong 250022, People’s Republic of China; 4Department of General Surgery, People’s Hospital of Central District of Jinan, Shandong 250022, People’s Republic of ChinaCorrespondence: Bin LiDepartment of Gastroenterology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, No. 324, Jingwuweiqi Road, Jinan, Shandong, People’s Republic of ChinaEmail [email protected]: Esophageal squamous cell carcinoma (ESCC) is the predominant type of esophageal carcinoma with a low survival rate and a poor prognosis. Therefore, it is of great significance to explore the effective tumor markers in early diagnosis, treatment monitoring and prognosis evaluation of ESCC. The current study was designed to explore the important role of β-arrestin1 in ESCC and the underlying mechanism.Methods: The defined effects of β-arrestin1 on cell proliferation, migration, invasion, EMT and tumor growth were investigated both in ESCC cells and in vivo model of ESCC. β-arrestin1 expression was detected using Western blot and immunohistochemistry assay. The cell proliferation ability was determined using CCK-8 assay. Wound healing assay and trans-well invasion assay were performed to determine cell migration and invasion. The key proteins related to cell migration, invasion and EMT were detected by Western blot. Tumor growth in vivo was also monitored by tumor volume and weight. In addition, the effects of β-arrestin1 on AKT/GSK3β/β-catenin pathway were evaluated.Results: β-arrestin1 was aberrantly upregulated in human ESCC tissues, ESCC cell lines and animal model of ESCC. β-arrestin1 downregulation inhibited cell proliferation, migration, invasion and EMT of ESCC in vitro and vivo. β-arrestin downregulation also suppressed tumor growth in vivo model of ESCC. In addition, the inhibitory effects of β-arrestin1 downregulation were exerted via AKT/GSK3β/β-catenin signaling pathway.Discussion: The results in the present study together confirmed the truth that β-arrestin1 interference may suppress ESCC cell proliferation, migration, invasion, EMT and tumor growth via AKT/GSK3β/β-catenin signaling pathway.Keywords: β-arrestin1, proliferation, invasion, migration, EMT, tumor growth
