Basic Study
Copyright ©The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 21, 2022; 28(35): 5141-5153
Published online Sep 21, 2022. doi: 10.3748/wjg.v28.i35.5141
Long noncoding RNA negative regulator of antiviral response contributes to pancreatic ductal adenocarcinoma progression via targeting miR-299-3p
Hai-Quan Wang, Chun-Hua Qian, Zeng-Ya Guo, Pei-Ming Li, Zheng-Jun Qiu
Hai-Quan Wang, Zheng-Jun Qiu, Department of General Surgery, Shanghai General Hospital of Nanjing Medical University, Shanghai 200080, China
Hai-Quan Wang, Zeng-Ya Guo, Pei-Ming Li, Zheng-Jun Qiu, Department of General Surgery, Shanghai Jiao Tong University School of Medicine, Shanghai 200080, China
Chun-Hua Qian, Department of Endocrinology and Metabolism, Shanghai Tenth People’s Hospital, Shanghai 200072, China
Author contributions: Qiu ZJ and Wang HQ designed the experiments and revised the manuscript; Qian CH and Wang HQ performed most of the experiments; Li PM and Guo ZY analyzed the data; Wang HQ and Guo ZY wrote the manuscript; all authors discussed the results and reviewed the manuscript.
Supported by the National Natural Science Foundation of China, No. 81974372.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee of the Animal Ethics Committee of Shanghai General Hospital, No. SHDSYY-2020-T1663.
Conflict-of-interest statement: There are no conflicts of interest to report.
Data sharing statement: The authors are amenable to data sharing.
ARRIVE guidelines statement: The authors have read the ARRIVE Guidelines, and the manuscript was prepared and revised according to the ARRIVE Guidelines.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Zheng-Jun Qiu, MD, Chief Doctor, Director, Surgeon, Department of General Surgery, Shanghai General Hospital of Nanjing Medical University, No. 100 Haining Road, Shanghai 200080, China. qiuzjdoctor@sina.com
Received: November 9, 2021
Peer-review started: November 9, 2021
First decision: April 16, 2022
Revised: April 28, 2022
Accepted: September 1, 2022
Article in press: September 1, 2022
Published online: September 21, 2022
ARTICLE HIGHLIGHTS
Research background

Pancreatic ductal adenocarcinoma (PDAC) has high malignancy and poor prognosis. Long noncoding RNAs (lnRNAs) are recognized as crucial factors and associated with progression of PDAC. However, the specific biological role and practical clinical significance of lnRNAs and negative regulator of antiviral response (NRAV) in PDAC remain unclear.

Research motivation

Early and timely diagnosis and treatment of PDAC are still scarce. Therefore, it is a matter of urgency to comprehensively understand the pathogenesis of PDAC and explore more effective targets for its diagnosis and treatment.

Research objectives

To study the role of NRAV in the growth and metastasis of PDAC.

Research methods

Real-time polymerase chain reaction detected expression of NRAV and miR-299-3p in PDAC cells. The temperament correction and miR-299-3p in the process of cell proliferation, metastasis and invasion were verified by Cell Counting Kit-8, precipitation test, and Transwell assay. RNA and fluorescent enzyme immunoprecipitation test to test the interaction between NRAV and miR-299-3p. Verify the interaction between NRAV and miR-299-3p.

Research results

According to our data, NRAV in PDAC was significantly increased, which is related to the negative survival rate of PDAC patients. NRAV overexpression was conducive to the proliferation and metastasis of PDAC cells, and NRAV knockout reversed these effects. Finally, in terms of mechanism, NRAV acts as a miR-299-3p molecular sponge. Overexpression of miR-299-3p significantly changed the role of NRAV in the proliferation, metastasis and invasion of PDAC cells.

Research conclusions

NRAV promotes proliferation and metastasis of PDAC by playing the molecule sponge function of miR-299-3p.

Research perspectives

NRAV facilitated the progression of PDAC, which provides a potential biological marker for diagnosis and therapeutic target for PDAC.