Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

Shi, Zhenfeng; Zhang, Hao; Song, Jie; Yang, Xinggang; Huang, Qunxiong; Mao, Yunfei; Zhang, Yan

doi:10.1002/jgm.3309

Cited by 18 publications

(9 citation statements)

References 34 publications

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“…The dysregulated lncRNAs probably modulate tumorigenesis and other biological functions (28)(29)(30). Our result is consistent with others' reports that SNHG8 is associated with the progression in multiple types of cancer in the liver, colon, lung, ovary, prostate, esophagus, and so on (15,(31)(32)(33)(34)(35). Our data support that the acting mechanism of SNHG8 could be multiple: (1) it activated BCL-2, preventing GC cells from apoptosis; (2) it activated CCND1, regulating the cell cycle; and (3) it activated CDH1, CDH2Snai1, and VIM, enhancing the epithelial-mesenchymal transition, thus promoting the migration, invasion, and metastasis of GC cells.…”

Section: Discussionsupporting

confidence: 92%

SNHG8 Promotes the Progression of Epstein–Barr Virus-Associated Gastric Cancer via Sponging miR-512-5p and Targeting TRIM28

Zou

Liu

et al. 2021

Front. Oncol.

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SNHG8, a family member of small nucleolar RNA host genes (SNHG), has been reported to act as an oncogene in gastric carcinoma (GC). However, its biological function in Epstein–Barr virus (EBV)-associated gastric cancer (EBVaGC) remains unclear. This study investigated the role of SNHG8 in EBVaGC. Sixty-one cases of EBVaGC, 20 cases of non-EBV-infected gastric cancer (EBVnGC), and relative cell lines were studied for the expression of SNHG8 and BHRF1 (BCL2 homolog reading frame 1) encoded by EBV with Western blot and qRT-PCR assays. The relationship between the expression levels of SNHG8 and the clinical outcome in 61 EBVaGC cases was analyzed. Effects of overexpression or knockdown of BHRF1, SNHG8, or TRIM28 on cell proliferation, migration, invasion, and cell cycle and the related molecules were determined by several assays, including cell proliferation, colony assay, wound healing assay, transwell invasion assay, cell circle with flow cytometry, qRT-PCR, and Western blot for expression levels. The interactions among SNHG8, miR-512-5p, and TRIM28 were determined with Luciferase reporter assay, RNA immunoprecipitation (RIP), pull-down assays, and Western blot assay. The in vivo activity of SNHG8 was assessed with SNHG8 knockdown tumor xenografts in zebrafish. Results demonstrated that the following. (1) BHRF1 and SNHG8 were overexpressed in EBV-encoded RNA 1-positive EBVaGC tissues and cell lines. BHRF1 upregulated the expressions of SNHG8 and TRIM28 in AGS. (2) SNHG8 overexpression had a significant correlation with tumor size and vascular tumor thrombus. Patients with high SNHG8 expression had poorer overall survival (OS) compared to those with low SNHG8 expression. (3) SNHG8 overexpression promoted EBVaGC cell proliferation, migration, and invasion in vitro and in vivo, cell cycle arrested at the G2/M phase via the activation of BCL-2, CCND1, PCNA, PARP1, CDH1, CDH2 VIM, and Snail. (4) Results of dual-luciferase reporter assay, RNA immunoprecipitation, and pull-down assays indicated that SNHG8 sponged miR-512-5p, which targeted on TRIM28 and promoted cancer malignant behaviors of EBVaGC cells. Our data suggest that BHRF1 triggered the expression of SNHG8, which sponged miR-512-5p and upregulated TRIM28 and a set of effectors (such as BCL-2, CCND1, CDH1, CDH2 Snail, and VIM) to promote EBVaGC tumorigenesis and invasion. SNHG8 could be an independent prognostic factor for EBVaGC and sever as target for EBVaGC therapy.

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Section: Discussionsupporting

confidence: 92%

SNHG8 Promotes the Progression of Epstein–Barr Virus-Associated Gastric Cancer via Sponging miR-512-5p and Targeting TRIM28

Zou

Liu

et al. 2021

Front. Oncol.

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“…Accumulating studies have shown that lncRNAs exert their biological roles by acting as miRNA sponges [ 30 , 31 ]. For example, lncRNA SNHG8 is reported to contribute to the development of prostate cancer by elevating HOXB7 expression via sponging miR-384 [ 32 ]. lncRNA MCM3AP-AS1 is reported to restrain the development of colorectal cancer through mediating miR-19a-3p/FOXF2 signaling [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA CASC2 restrains high glucose-induced proliferation, inflammation and fibrosis in human glomerular mesangial cells through mediating miR-135a-5p/TIMP3 axis and JNK signaling

Dong-ju

Xue

2021

Diabetol Metab Syndr

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Background Diabetic nephropathy (DN) is a common complication of diabetes. Long non-coding RNA (lncRNA) cancer susceptibility candidate 2 (CASC2) is reported to exert a protective role in DN by a previous study. The working mechanism underlying the protective role of CASC2 in DN progression was further explored in this study. Methods The expression of CASC2 and microRNA-135a-5p (miR-135a-5p) was determined by real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation ability was assessed by Cell Counting Kit-8 (CCK8) assay and 5-ethynyl-29-deoxyuridine (EDU) assay. Enzyme-linked immunosorbent assay (ELISA) was conducted to analyze the production of inflammatory cytokines in the supernatant. Western blot assay was performed to analyze protein expression. Dual-luciferase reporter assay and RNA immunoprecipitation (RIP) assay were performed to verify the target relationship between miR-135a-5p and CASC2 or tissue inhibitors of metalloproteinase 3 (TIMP3). Results High glucose (HG) treatment reduced the expression of CASC2 in human glomerular mesangial cells (HMCs) in a time-dependent manner. CASC2 overexpression suppressed HG-induced proliferation, inflammation and fibrosis in HMCs. miR-135a-5p was validated as a target of CASC2, and CASC2 restrained HG-induced influences in HMCs partly by down-regulating miR-135a-5p. miR-135a-5p bound to the 3ʹ untranslated region (3ʹUTR) of TIMP3, and CASC2 positively regulated TIMP3 expression by sponging miR-135a-5p in HMCs. miR-135a-5p silencing inhibited HG-induced effects in HMCs partly by up-regulating its target TIMP3. CASC2 overexpression suppressed HG-induced activation of Jun N-terminal Kinase (JNK) signaling partly through mediating miR-135a-5p/TIMP3 signaling. Conclusions In conclusion, CASC2 alleviated proliferation, inflammation and fibrosis in DN cell model by sponging miR-135a-5p to induce TIMP3 expression.

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“…35 Small Nucleolar RNA Host Gene 8 (SNHG8) can promote the proliferation and migration of multiple tumor cells through serving as sponge for different miRNAs. [36][37][38] Our results revealed that the ARHGAP22-IT1 and SNHG8 were overexpressed in TAD patients. According to the ceRNA hypothesis, the ARHGAP22-IT1 and SNHG8 can competitively bind to hsa-miR-3202 and upregulate SLC7A5, thus promoting VSMC proliferation and TAD development.…”

Section: Discussionmentioning

confidence: 57%

Construction and Integrated Analysis of Competitive Endogenous Long Non-Coding RNA Network in Thoracic Aortic Dissection

Shao¹,

Luo²,

Liu³

et al. 2021

IJGM

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Background: Long non-coding RNAs (lncRNAs) can act as a competitive endogenous RNA (ceRNA) to regulate gene expression by sequestering the microRNA (miRNA). However, the lncRNA-miRNA-mRNA ceRNA network in thoracic aortic dissection (TAD) has been rarely documented. Methods: Three Gene Expression Omnibus (GEO) datasets were used to detect differentially expressed mRNAs, miRNAs, and lncRNAs in TAD. Gene ontology and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were conducted for the differentially expressed mRNAs. A protein-protein interaction network for differentially expressed mRNAs was also constructed, and hub genes were identified. We established a ceRNA network of TAD based on the differentially expressed miRNAs, mRNAs and lncRNAs, and verified our results using an independent dataset and quantitative real-time PCR (qRT-PCR). Results: In TAD, 267 lncRNAs, 81 miRNAs, and 346 mRNAs were identified as differentially expressed. The established ceRNA network consisted of seven lncRNA nodes, three mRNA nodes, and three miRNA nodes, and the expression of miRNAs in TAD was opposite to that of lncRNAs and mRNAs. Subsequently, an independent GEO dataset and qRT-PCR were used to validate the expression of three mRNAs. In addition, the expression differences in SLC7A5, associated miRNA and lncRNA were verified. According to gene set enrichment analysis of SLC7A5, the most significant KEGG pathway was considerably enriched in spliceosome and pentose phosphate pathway. Conclusion:We established a novel ceRNA regulatory network in TAD, which provides valuable information for further research in the molecular mechanisms of TAD.

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Long non‐coding RNA SNHG8 promotes prostate cancer progression through repressing miR‐384 and up‐regulating HOXB7

Cited by 18 publications

References 34 publications

SNHG8 Promotes the Progression of Epstein–Barr Virus-Associated Gastric Cancer via Sponging miR-512-5p and Targeting TRIM28

SNHG8 Promotes the Progression of Epstein–Barr Virus-Associated Gastric Cancer via Sponging miR-512-5p and Targeting TRIM28

Long non-coding RNA CASC2 restrains high glucose-induced proliferation, inflammation and fibrosis in human glomerular mesangial cells through mediating miR-135a-5p/TIMP3 axis and JNK signaling

Construction and Integrated Analysis of Competitive Endogenous Long Non-Coding RNA Network in Thoracic Aortic Dissection

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