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.
Highlights
Gastric cancer (GC) is the fifth most common cancer and third leading cause of cancer death globally, being prevalent in Asia [1]
We initially analyzed the expression level of the pseudogene-derived long noncoding RNAs (lncRNAs) DUXAP8 in human GC tissues by using microarray data downloaded from the Gene Expression Omnibus (GEO; GSE58828[23] and GSE13861[24]), and found that the DUXAP8 expression level was significantly upregulated in GC tissues compared with that in normal tissues (Figure 1A)
To determine the relationship between DUXAP8 expression and the prognosis of GC patients after gastrectomy, progression-free survival (PFS) and overall survival (OS) curves were plotted according to DUXAP8 expression level and analyzed by the Kaplan– Meier method and log-rank test, respectively (Figure 1D and 1E)
Summary
Gastric cancer (GC) is the fifth most common cancer and third leading cause of cancer death globally, being prevalent in Asia [1]. More than half of patients are diagnosed at an advanced stage, which is passed the optimal time for a radical operation [2,3,4]. Great progress has been made in research on GC, the basic molecular mechanisms behind its development are still poorly understood. There remains an urgent need to decipher the different mechanisms involved in GC progression. Many oncogenes and tumor suppressors have been identified as key players in GC tumorigenesis and development; no appropriate molecular biomarkers have been established to facilitate the comprehensive management of patients, for example, via prognostic prediction [5]. The exploration of new indicators of GC diagnosis and novel treatment targets is increasingly important
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