Home Neoplasma 2018 Neoplasma Vol.65, No.6, p.933-942, 2018

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.65, No.6, p.933-942, 2018

Title: Long noncoding RNA LINC00313 modulates papillary thyroid cancer tumorigenesis via sponging miR-4429
Author: W.J. WU, H. YIN, J.J. HU, X.Z. WEI

Abstract: Mounting evidence indicates that long noncoding RNAs (lncRNAs) play a critical role in tumorigenesis. LncRNA LINC00313 has been found to be up-regulated and associated with poor prognosis in lung cancer. However, the potential role and clinical value of LINC00313 in human papillary thyroid cancer (PTC) remain elusive and therefore require examination. The aim of this study is to investigate the role of LINC00313 in papillary thyroid cancer (PTC). We found its expression was significantly up-regulated in PTC tissues and cell lines and that this up-regulation correlated with poor prognosis. In vitro experiments indicated that down-regulation of LINC00313 inhibited proliferation and the migratory and colony-forming abilities of PTC cells. Moreover, silencing LINC00313 induced cell cycle arrest and apoptosis in the PTC cells. In addition, mechanism studies showed that LINC00313 down-regulates miR-4429 expression, and that miR-4429 over-expression can abrogate the oncogenic role of LINC00313 in PTC cells. In summary, our data revealed that LINC00313 acts as an oncogene in PTC via sponging miR-4429, and this suggests that LINC00313 may be successfully applied as a therapeutic target in PTC.

Keywords: LINC00313, papillary thyroid cancer, miR-4429, cell cycle arrest, apoptosis
Published online: 18-Jun-2018
Year: 2018, Volume: 65, Issue: 6 Page From: 933, Page To: 942

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.