Oncotarget

Research Papers:

The pseudogene derived long noncoding RNA DUXAP8 promotes gastric cancer cell proliferation and migration via epigenetically silencing PLEKHO1 expression

Hong-Wei Ma, Min Xie, Ming Sun, Tian-Yu Chen, Rong-Rong Jin, Tian-Shi Ma, Qin-Nan Chen, Er-Bao Zhang, Xue-Zhi He, Wei De and Zhi-Hong Zhang _

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Oncotarget. 2017; 8:52211-52224. https://doi.org/10.18632/oncotarget.11075

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Abstract

Hong-wei Ma1,*, Min Xie2,4,*, Ming Sun2, Tian-yu Chen1, Rong-rong Jin1, Tian-shi Ma1, Qin-nan Chen3, Er-bao Zhang2, Xue-zhi He2, Wei De2 and Zhi-hong Zhang1

1Department of Pathology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China

2Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing, People’s Republic of China

3Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, People’s Republic of China

4Center for Reproduction and Genetics, Suzhou Municipal Hospital, Nanjing Medical University Affiliated Suzhou Hospital, Suzhou, People’s Republic of China

*These authors have contributed equally to this work

Correspondence to:

Zhi-hong Zhang, email: zhangzh@njmu.edu.cn

Keywords: gastric cancer, pseudogene, lncRNA, DUXAP8, PLEKHO1

Received: April 19, 2016    Accepted: July 19, 2016    Published: August 05, 2016

ABSTRACT

Gastric cancer (GC) is the third leading cause of cancer death due to its poor prognosis and limited treatment options. Evidence indicates that pseudogene-derived long noncoding RNAs (lncRNAs) may be important players in human cancer progression, including GC. In this paper, we report that a newly discovered pseudogene-derived lncRNA named DUXAP8, a 2107-bp RNA, was remarkably upregulated in GC. Additionally, a higher level of DUXAP8 expression in GC was significantly associated with greater tumor size, advanced clinical stage, and lymphatic metastasis. Patients with a higher level of DUXAP8 expression had a relatively poor prognosis. Further experiments revealed that knockdown of DUXAP8 significantly inhibited cell proliferation and migration, as documented in the SGC7901 and BGC823 cell lines. Furthermore, RNA immunoprecipitation and chromatin immunoprecipitation assays demonstrated that DUXAP8 could epigenetically suppress the expression of PLEKHO1 by binding to EZH2 and SUZ12 (two key components of PRC2), thus promoting GC development. Taken together, our findings suggest that the pseudogene-derived lncRNA DUXAP8 promotes the progression of GC and is a potential therapeutic target for GC intervention.


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