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MicroRNA-320d regulates tumor growth and invasion by promoting FoxM1 and predicts poor outcome in gastric cardiac adenocarcinoma.
- Source :
-
Cell & Bioscience . 6/16/2020, Vol. 10 Issue 1, p1-13. 13p. - Publication Year :
- 2020
-
Abstract
- Recent evidences demonstrate that dysregulated expression of microRNA-320d (miR-320d) has been associated with several cancer development and progression. However the effect of miR-320d on gastric cardiac adenocarcinoma (GCA) and the association of miR-320d with its potential gene target FoxM1 remain unclear. Here, we evaluated expression profile of miR-320d and FoxM1 in 60 human GCA tissues and GCA cell lines (OE-19 and SK-GT2). Immunohistochemistry, qualitative PCR and western-blotting were performed in GCA tissues to detect the expression level of miR-320d and FoxM1. CCK-8, transwell, wound-healing assays, and in vivo experiments were conducted using GCA cells that treated with miR-320d mimics or inhibitors to evaluate the biological functions of miR-320d. Luciferase reporter assay was conducted to confirm possible binding sites of FoxM1 for miR-320d. Compared with paired non-cancerous tissues, it showed that miR-320d expression was significantly decreased in GCA specimens (P < 0.0001), while FoxM1 was significantly upregulated in GCA tissues (P < 0.0001). Modulating miR-320d function by transfection of miR-320 mimics or inhibitor led to inhibition or promotion of GCA cell proliferation and invasion, thus regulating tumor progression in GCA-tumor bearing mice. The mechanism analysis of miR-320d/FoxM1 showed that FoxM1 has two miR-320d binding sites in its 3′-untranslated region (3′-UTR), that contributes to regulation of the cell biological behaviors. Taken together, our data suggested that miR-320d acts as a tumor suppressor in GCA by directly targeting FoxM1 and thus potentially serves as a biomarker for anti-GCA therapy in GCA patients. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 20453701
- Volume :
- 10
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Cell & Bioscience
- Publication Type :
- Academic Journal
- Accession number :
- 143802057
- Full Text :
- https://doi.org/10.1186/s13578-020-00439-7