4.6 Article

sMicroRNA-1290 inhibits cells proliferation and migration by targeting FOXA1 in gastric cancer cells

Journal

GENE
Volume 582, Issue 2, Pages 137-142

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.gene.2016.02.001

Keywords

Gastric cancer; miR-1290; Proliferation; Migration; Apoptosis; FOXA1

Funding

  1. [2013YZ0002]

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Background/Aims: Gastric cancer is the third leading cause of cancer-related deaths in the world with high mortality rate due to the lack of markers in early detection and effective therapies. MicroRNAs (miRNAs), a critical part of epigenetic regulations in tumor, have been shown to be closely related to the initiation, development, invasion, metastasis and prognosis of gastric cancer. The present study aims to investigate the expression of miR-1290 in gastric tumor cells and to elucidate the target gene of miR-1290 in SGC-7901 gastric cancer cells. Methodology: The fluorescence in situ hybridization, real time PCR and Western blot were used to investigate the expression of miR-1290 in gastric tumor cells and clinical gastric tumor samples. The effect of miR-1290 expression on gastric tumor cells was studied using Synthetic miR-1290 inhibitor transfection, in vitro wound healing assay and flow cytometry analysis. Bioinformatics and Luciferase reporter assay were used to predict and validate the target gene of miR-1290. Results: Our results revealed that miR-1290 was highly expressed in SGC-7901 gastric cancer cells as well as in clinical gastric cancer samples, which was correlated with clinical stages, depth of invasion and lymph node metastasis. Synthetic miR-1290 inhibitor transfection significantly inhibited the proliferation and migration of SGC-7901 cells. Bioinformatics analysis and luciferase reporter assay suggested that miR-1290 functioned in gastric cancer cells by targeting FOXA1 gene. Conclusion: miR-1290 promotes gastric tumor cells proliferation and metastasis through FOXA1, which could be used as a marker for diagnosis and a target for therapeutic intervention. (C) 2016 Elsevier B.V. All rights reserved.

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