Back to Journals » OncoTargets and Therapy » Volume 12

Pseudogene DUXAP10 acts as a diagnostic and prognostic marker and promotes cell proliferation by activating PI3K/AKT pathway in hepatocellular carcinoma

Authors Yue C, Liang C, Ge H, Yan L, Xu Y, Li G, Li P, Wei Z, Wu J

Received 30 March 2019

Accepted for publication 16 May 2019

Published 11 June 2019 Volume 2019:12 Pages 4555—4566

DOI https://doi.org/10.2147/OTT.S210623

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Ms Shreya Arora

Peer reviewer comments 2

Editor who approved publication: Dr William Cho


Chaosen Yue,1,* Chaojie Liang,2,* Hua Ge,1 Lijun Yan,1 Yingchen Xu,1 Guangming Li,1 Pengyang Li,3 Zhigang Wei,2 Jixiang Wu1

1Department of General Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, People’s Republic of China; 2Department of General Surgery, First Hospital/First Clinical Medical College of Shanxi Medical University, Taiyuan, Shanxi, People’s Republic of China; 3Department of Medicine, Saint Vincent Hospital, Worcester, MA, USA

*These authors contributed equally to this work

Background: Recently, the pseudogene DUXAP10 was shown to be overexpressed in various human cancers and emerged as a key cancer regulator. However, the roles of DUXAP10 in hepatocellular carcinoma (HCC) tumorigenesis and progression remain uncharacterized.
Methods: Comprehensive analyses were performed to investigate DUXAP10 expression patterns, potential biologic functions, and clinical significance in HCC based on the data downloaded from the Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. DUXAP10 expression levels in HCC tissue sections and cells were verified using quantitative real-time PCR analysis. DUXAP10-siRNA was used to silence DUXAP10 in the Hep3B cell line to determine the roles of DUXAP10 in HCC cell proliferation.
Results: DUXAP10 was significantly overexpressed in HCC, and DUXAP10 upregulation was closely associated with poor prognoses in HCC patients. DUXAP10 knockdown decreased cell proliferation and arrested HCC cells in the G1 phase of the cell cycle. Western blot analysis showed that DUXAP10 knockdown decreased p-AKT expression in HCC cells.
Conclusion: Our study demonstrates that pseudogene DUXAP10 promotes HCC cell proliferation by activating PI3K/AKT pathway and could act as a potential diagnostic and prognostic biomarker for HCC patients.

Keywords: DUXAP10, HCC, biomarker

Creative Commons License This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

Download Article [PDF]  View Full Text [HTML][Machine readable]