Long noncoding RNA SNHG20 promotes prostate cancer progression via upregulating DDX17

Abstract

Introduction: Accumulating evidence has revealed the critical roles of long noncoding RNAs (lncRNAs) in various cancers. LncRNA SNHG20 has been shown to be a cancer-associated lncRNA in several cancers with diverse mechanisms. However, the clinical references, biological roles, and mechanisms of action of SNHG20 in prostate cancer (PCa) are still unclear. Material and methods: The expression of SNHG20 in PCa tissues and cell lines was detected by RT-qPCR. The correlations between SNHG20 expression and clinicopathological features were analyzed by χ 2 test. The roles of SNHG20 in PCa cell proliferation and migration were detected by CCK-8, EdU incorporation, and transwell assays. The regulatory mechanisms of SNHG20 on DDX17 were detected by dual luciferase reporter assay, RT-qPCR, and western blot. Results: SNHG20 is highly expressed in PCa tissues and cell lines. High expression of SNHG20 is positively correlated with high Gleason score and advanced tumor stage. Functional experiments revealed that overexpression of SNHG20 promotes PCa cell proliferation and migration. SNHG20 knockdown represses PCa cell proliferation and migration. Mechanistically, SNHG20 was verified to act as a competing endogenous RNA (ceRNA) to upregulate DDX17. DDX17 is also highly expressed and has oncogenic roles in PCa. Furthermore, the expression of DDX17 is significantly positively correlated with that of SNHG20 in PCa tissues. Depletion of DDX17 reverses the oncogenic roles of SNHG20 in PCa. Conclusions: These data showed that SNHG20 promotes PCa cell proliferation and migration via acting as a ceRNA to upregulate DDX17. This study also suggested that SNHG20 may be a potential novel therapeutic target for PCa.

DDX17 modulates the expression and alternative splicing of genes involved in apoptosis and proliferation in lung adenocarcinoma cells

“…In this study, we showed that siRNA knockdown of DDX17 significantly inhibited proliferation and led to increased apoptosis in A549 cells. This oncogenic effect of DDX17 in LUAD is consistent with the results of studies on other cancer types ( Xue et al, 2019 ; Shin et al, 2007 ; Wu et al, 2021 ).…”

DDX17 modulates the expression and alternative splicing of genes involved in apoptosis and proliferation in lung adenocarcinoma cells

“…In addition, using TCGA data, we showed that high DDX17 expression was associated with poor survival in LUAD patients. This oncogenic effect of DDX17 in LUAD is consistent with the results of studies on other cancer types 13,14,45 .…”

DDX5 and DDX17—multifaceted proteins in the regulation of tumorigenesis and tumor progression

“…Except for liver cancer ( 2 ) and pancreatic ductal adenocarcinoma ( 3 ), DDX5 is overexpressed in most tumors, such as breast cancer ( 4 ), prostate cancer ( 5 ), endometrial cancer ( 6 ), gastric cancer ( 7 ), esophageal cancer ( 8 ), colorectal cancer ( 9 ), glioma ( 10 ), lung adenocarcinoma ( 11 ), cervical squamous cell carcinoma ( 12 ), and non-small cell lung cancer (NSCLC) ( 13 ) etc. DDX17 is also overexpressed in many tumors, such as drug (gefitinib)-resistant NSCLC ( 14 ), prostate cancer ( 15 ), breast cancer ( 16 ), glioma ( 17 ), and hepatocellular carcinoma ( 18 ) etc. Therefore, DDX5 and DDX17 are potential targets for cancer therapy.…”