Home Neoplasma 2016 Neoplasma Vol.63, No.6, p.873-879,2016

Journal info

6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal

Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.63, No.6, p.873-879,2016

Title: MicroRNA-520f suppresses growth of gastric carcinoma cells by target ATPase family AAA domain-containing protein 2 (ATAD2)
Author: S. HONG, M. BI, S. CHEN, P. ZHAO, B. LI, D. SUN, J. TAI

Abstract: MicroRNAs (miRNAs) are small, non-coding RNAs that can serve as tumor suppressor genes or oncogenes in tumorigenesis. More and more evidence demonstrate that abnormal expression of miRNAs lead to the gastric carcinoma occurrence. In the present study, we revealed that the expression levels of miR-520f were significantly down-regulated in gastric carcinoma cells and clinical gastric carcinoma samples. Next, we demonstrated that introduction of miR-520f inhibited the growth of gastric carcinoma cells in vitro. However, down-regulate the expression levels of miR-520f by anti-miR-520f lead to an enhanced cell proliferation, implying that miR-520f maybe serve as a novel tumor suppressor. Moreover, we found that ATPase family AAA domain-containing protein 2 (ATAD2) was one target genes of miR-520f downstream regulator, which caused the decreased expression of ATAD2. Meanwhile, the overexpression of ATAD2 reversed the inhibited proliferation ability caused by miR-520f. Therefore, our find that miR-520f involves in gastric carcinoma proliferation, pointing a therapeutic probability of miR-520f in the therapy of gastric carcinoma.

Keywords: MicroRNA-520f, gastric carcinoma, ATAD2, proliferation
Published online: 16-Nov-2016
Year: 2016, Volume: 63, Issue: 6 Page From: 873, Page To: 879

download file

© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.