Home HOME Neoplasma 2017 Neoplasma Vol.64, No.1, p.40-47,2017

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.64, No.1, p.40-47,2017

Title: miR-508-5p acts as an anti-oncogene by targeting MESDC1 in hepatocellular carcinoma
Author: S. G. WU, Y. J. HUANG, B. BAO, L. M. WU, J. DONG, X. H. LIU, Z. H. LI, X. Y. WANG, L. WANG, B. J. CHEN, W. CHEN

Abstract: Hepatocellular carcinoma (HCC) is the third leading cause of cancer associated mortality. Accumulating evidence has shown that microRNAs (miRNAs) act as critical factors for tumor recurrence and metastasis. MiR-508-5p has been reported as a down-regulated miRNA in the primary gastric cancer tissues. However, the role of miR-508-5p on HCC has not been well elucidated. In this study, we observed that miR-508-5p was downregulated in HCC tissues when compared to the non-tumorous tissues. We then demonstrated that overexpression of miR-508-5p attenuated HepG2 cells proliferation and invasion and induced cell apoptosis in vitro. Furthermore, our further investigations revealed that mesoderm development candidate 1 (MESDC1) is a potential target of miR-508-5p, as well as miR-508-5p overexpression downregulated MESDC1 expression. Overexpression of MESDC1 promoted HepG2 cells migration, invasion and proliferation in vitro. In addition, miR-508-5p markedly suppressed the tumor growth in xenograft model, while MESDC1 promoted the tumor growth in xenograft model. This study provides new insight into molecular mechanisms that miR-508-5p acts as a tumor suppressor by targeting MESDC1 in HCC progression.

Keywords: miR-508-5p, MESDC1, hepatocellular carcinoma
Published online: 10-Jan-2017
Year: 2017, Volume: 64, Issue: 1 Page From: 40, Page To: 47
doi:10.4149/neo_2017_105


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.