MiRNA-373 Promotes Urinary Bladder Cancer Cell Proliferation, Migration and Invasion Through Upregulating Epidermal Growth Factor Receptor

Overview

Journal Exp Ther Med

Specialty Pathology

Date 2019 Jan 26

PMID 30679992

Citations 10

Authors

Yibing Wang

Zhenqun Xu

Xia Wang

Affiliations

Soon will be listed here.

Abstract

MicroRNA (miRNA)-373 has been demonstrated to be involved in several types of cancer, whereas its involvement in urinary bladder cancer and the mechanism of its function remains poorly understood. The present study aimed to investigate the functionality of miRNA-373 in urinary bladder cancer. Tumor tissues and adjacent healthy tissues were collected from patients with urinary bladder cancer (n=55), and blood samples were collected from patients with urinary bladder cancer and healthy controls (n=45). The expression of miRNA-373 in these tissues was detected by reverse transcription quantitative polymerase chain reaction. The diagnostic value of serum miRNA-373 for urinary bladder cancer was investigated by receiver operating characteristic curve analysis and survival curve analysis, respectively. miRNA-373 mimics were transfected into urinary bladder cancer cells, and the effects on cancer cell proliferation, migration and invasion, and on epidermal growth factor receptor (EGFR) expression was assessed by Cell Counting kit-8 assay, Transwell migration and invasion assays, and western blot analysis. It was identified that the miRNA-373 expression level was increased in tumor tissues compared with adjacent healthy tissues. The serum level of miRNA-373 was increased in patients with cancer compared with the healthy controls. Serum miRNA-373 may be used to accurately predict urinary bladder cancer. miRNA-373 overexpression promoted tumor cell proliferation, migration and invasion, and resulted in upregulated EGFR expression in urinary bladder cancer cells. It was concluded that miRNA-373 overexpression may promote urinary bladder cancer cell proliferation, migration and invasion by upregulating EGFR.

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