Literature DB >> 30107990

LncRNA UCA1 sponges miR-204-5p to promote migration, invasion and epithelial-mesenchymal transition of glioma cells via upregulation of ZEB1.

Chao Liang1, Yang Yang2, Junhong Guan3, Tao Lv3, Shengtao Qu3, Qiang Fu3, Hongyu Zhao4.   

Abstract

Long non-coding RNA urothelial carcinoma associated 1 (lncRNA UCA1) promotes cancer progression and enhances chemoresistance through miR-204-5p in a few cancers. However, no studies have investigated whether UCA1 regulates glioma metastasis through miR-204-5p and its target. In the present study, cell migration, invasion and epithelial-mesenchymal transition (EMT) were evaluated in glioma cells overexpressing UCA1. The relationships among UCA1, miR-204-5p and ZEB1 were examined by real-time PCR, western blotting and dual-luciferase reporter assays. The effect of UCA1 knockdown on xenograft tumor growth was investigated. The levels of miR-204-5p, fibronectin, COL5 A1 and ZEB1 in tumor tissues were also determined. The results showed that UCA1 overexpression promoted cell migration, invasion and EMT. UCA1 interacted with miR-204-5p and decreased its level. ZEB1 was identified as a direct target of miR-204-5p and miR-204-5p negatively regulated ZEB1 expression. Moreover, UCA1 sponged miR-204-5p and partially rescued the inhibitory effect of miR-204-5p on ZEB1. In our in vivo studies, UCA1 knockdown reduced tumor volume and tumor weight. In addition, the levels of fibronectin, COL5 A1 and ZEB1 were decreased, while miR-204-5p level was increased. The present study provides the first evidence that UCA1 promotes glioma metastasis through the miR-204-5p/ZEB1 axis, contributing to the understanding of the pathogenesis of glioma.
Copyright © 2018. Published by Elsevier GmbH.

Entities:  

Keywords:  Glioma; Metastasis; UCA1; ZEB1; miR-204-5p

Mesh:

Substances:

Year:  2018        PMID: 30107990     DOI: 10.1016/j.prp.2018.07.036

Source DB:  PubMed          Journal:  Pathol Res Pract        ISSN: 0344-0338            Impact factor:   3.250


  18 in total

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