HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Graduate School of Medicine / Faculty of Medicine >
Peer-reviewed Journal Articles, etc >

MicroRNA-361-Mediated Inhibition of HSP90 Expression and EMT in Cervical Cancer Is Counteracted by Oncogenic lncRNA NEAT1

This item is licensed under:Creative Commons Attribution 4.0 International

Files in This Item:
cells-09-00632 (4).pdf1.68 MBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/76908

Title: MicroRNA-361-Mediated Inhibition of HSP90 Expression and EMT in Cervical Cancer Is Counteracted by Oncogenic lncRNA NEAT1
Authors: Xu, Daozhi Browse this author
Dong, Peixin Browse this author →KAKEN DB
Xiong, Ying Browse this author
Yue, Junming Browse this author
Konno, Yosuke Browse this author →KAKEN DB
Ihira, Kei Browse this author →KAKEN DB
Kobayashi, Noriko Browse this author
Todo, Yukiharu Browse this author →KAKEN DB
Watari, Hidemichi Browse this author →KAKEN DB
Keywords: microRNA-361
EMT
HSP90AA1
long non-coding RNA
NEAT1
cervical cancer
Issue Date: 5-Mar-2020
Publisher: MDPI
Journal Title: Cells
Volume: 9
Issue: 3
Start Page: 632
Publisher DOI: 10.3390/cells9030632
PMID: 32151082
Abstract: Epithelial-mesenchymal transition (EMT) is a key process contributing to cervical cancer (CC) metastasis, and microRNAs (miRNAs) modulate the expression of genes implicated in EMT. However, the accurate role of miR-361 in CC-associated EMT and the mechanisms underlying its function in CC remains largely unknown. The functional roles of miR-361 in CC cells were explored by a series of cell functional assays. Luciferase reporter assays were used to demonstrate the potential interaction between miR-361, HSP90, and long non-coding RNA (lncRNA) NEAT1. We detected a reduction of miR-361 expression in CC tissues compared with normal tissues, and miR-361 overexpression inhibited invasion and EMT phenotypes of CC cells by directly targeting a key EMT activator HSP90. Additionally, we detected significantly higher levels of HSP90 in CC tissues compared with normal tissues, and high expression of HSP90 predicted a poorer prognosis. We further identified NEAT1 as a significantly upregulated lncRNA in CC tissues and high expression of NEAT1 was associated with worse survival in CC patients. NEAT1 directly repressed miR-361 expression and played an oncogenic role in CC cell invasion and sphere formation. Conclusions: These results demonstrated that miR-361 directly targets HSP90 to inhibit the invasion and EMT features, and NEAT1 functions as an oncogenic lncRNA that suppresses miR-361 expression and induces EMT and sphere formation in CC cells, thus providing critical insights into the molecular pathways operating in this malignancy.
Rights: https://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/76908
Appears in Collections:医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 董 培新

Export metadata:

OAI-PMH ( junii2 , jpcoar_1.0 )

MathJax is now OFF:


 

 - Hokkaido University