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Current Molecular Pharmacology

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ISSN (Print): 1874-4672
ISSN (Online): 1874-4702

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Research Article

CircRNA 001418 Promoted Cell Growth and Metastasis of Bladder Carcinoma via EphA2 by miR-1297

Author(s): Guorui Peng, Hongxue Meng, Hongxin Pan and Wentao Wang*

Volume 14, Issue 1, 2021

Published on: 05 May, 2020

Page: [68 - 78] Pages: 11

DOI: 10.2174/1874467213666200505093815

Price: $65

Abstract

Background: Cancer is one of the major causes of human deaths at present. It is the leading cause of deaths in developed countries. Moreover, Circular RNAs (circRNAs) have been discovered to play important roles in tumor genesis and development and are abnormally expressed in bladder cancer .

Objective: The present study aims to investigate the anti-cancer effects of circ 001418 on bladder carcinoma and its possible mechanism.

Methods: Quantitative PCR (qPCR) and gene chip were used to measure the circ 001418 expression. Cell proliferation and transfer, apoptosis and caspase-8 and caspase-3 activity levels were measured using MTT, Transwell assay, Flow cytometry. Caspase-3 and 9 activity levels, EphA2, cytochrome c and FADD protein expression, were detected using Western blotting.

Results: The expression of circ 001418 was increased in patients with bladder carcinoma. Over-expression of circ 001418 promoted cell proliferation and transfer, and reduced apoptosis in vitro model of bladder carcinoma. Down-regulation of Circ 001418 inhibited cell proliferation and transfer, and induced apoptosis in vitro model of bladder carcinoma. Meanwhile, over-expression of circ 001418 induced EphA2 and cytochrome c protein expression, and suppressed FADD protein expression in vitro model of bladder carcinoma by the suppression of miR-1297. MiR-1297 reduced the pro-cancer effect of circ 001418 on apoptosis of bladder carcinoma.

Conclusion: Results showed that circRNA 001418 promoted cell growth and metastasis of bladder carcinoma via EphA2 by miR-1297.

Keywords: Circ 001418, bladder carcinoma, miR-1297, FADD, cytochrome c, EPHA2.

Graphical Abstract

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