ArticleOncoTargets and therapy2020
The Role of β-Arrestin1 in Esophageal Squamous Cell Carcinoma.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 2 citations in OpenAlex.
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
introductionEsophageal 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.
methodsThe 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.
resultsβ-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.
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