scholarly journals Long Noncoding RNA (lncRNA) Small Nucleolar RNA Host Gene 16 (SNHG16) Predicts Poor Prognosis and Sorafenib Resistance in Hepatocellular Carcinoma

2019 ◽  
Vol 25 ◽  
pp. 2079-2086 ◽  
Author(s):  
Zhenli Guo ◽  
Ju Zhang ◽  
Lulu Fan ◽  
Jiatao Liu ◽  
Hanqing Yu ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Poor Prognosis ◽  
Host Gene ◽  
Small Nucleolar Rna ◽  
Nucleolar Rna

scholarly journals Expression and gene regulatory network of SNHG1 in hepatocellular carcinoma

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Chaoran Zheng ◽  
Shicheng Yu
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Regulatory Network ◽  
Noncoding Rna ◽  
Host Gene ◽  
P Value ◽  
Tumour Suppressor Genes ◽  
Sequencing Data ◽  
Small Nucleolar Rna ◽  
Nucleolar Rna

Abstract Background Small nucleolar RNA host gene 1 (SNHG1), a long noncoding RNA (lncRNA), is a transcript that negatively regulates tumour suppressor genes, such as p53. Abnormal SNHG1 expression is associated with cell proliferation and cancer. We used sequencing data downloaded from Genomic Data Commons to analyse the expression and interaction networks of SNHG1 in hepatocellular carcinoma (HCC). Methods Expression was examined using the limma package of R and verified by Gene Expression Profiling Interactive Analysis. We also obtained miRNA expression data from StarBase to determine the lncRNA-miRNA-mRNA–related RNA regulatory network in HCC. Kaplan–Meier (KM) analysis was performed using the survival package of R. Gene Ontology annotation of genes was carried out using Metascape. Results We found that SNHG1 was overexpressed and often amplified in HCC patients. In addition, SNHG1 upregulation was associated with the promotion of several primary biological functions, including cell proliferation, transcription and protein binding. Moreover, we found similar trends of small nucleolar RNA host gene 1 (SNHG1), E2F8 (E2F transcription factor 8), FANCE (FA complementation group E) and LMNB2 (encodes lamin B2) expression. In the SNHG1-associated network, high expression levels of SNHG1 (log-rank P value = 0.0643), E2F8 (log-rank P value = 0.000048), FANCE (log-rank P value = 0.00125) and LMNB2 (log-rank P value = 0.0392) were significantly associated with poor survival. Single-cell analysis showed that E2F8 may play an important role in tumorigenesis or cancer development. Conclusions Our results highlight the benefit of utilizing multiple datasets to understand the functional potential regulatory networks of SNHG1 and the role of SNHG1 in tumours.

Long Noncoding RNA Small Nucleolar RNA Host Gene 6 Promotes Cell Proliferation, Migration and Invasion in Melanoma by Sponging miR-944

2021 ◽  
Vol 11 (8) ◽  
pp. 1459-1465
Author(s):  
Jinjin Zhu ◽  
Pan Xu
Keyword(s):  
Cell Proliferation ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Melanoma Cells ◽  
Host Gene ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Small Nucleolar Rna ◽  
Nucleolar Rna ◽  
A375 Cells

Long noncoding RNA small nucleolar RNA host gene 6 (SNHG6) has been reported to be a tumor promoter in various human cancers. Nevertheless, the detailed functions and clinical value of SNHG6 in melanoma remain elusive. The study aimed to investigate the role and potential mechanism of SNHG6 in melanoma metastasis. Quantitative real-time PCR (qRT-PCR) was used to detect the expressions of SNHG6 and miR-944 in melanoma cells. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) assay, and cell migration and invasion were measured by wound healing assay and cell invasion assay, respectively. In addition, dual luciferase reporter assay was performed to verify the interaction between SNHG6 and miR-944. The protein expressions of PI3K/Akt pathway were evaluated by western blot assay. The results revealed that SNHG6 expression was significantly increased in melanoma cells. Knockdown of SNHG6 suppressed cell proliferation, migration and invasion in A375 cells. Moreover, miR-944 was identified as a direct target of SNHG6 in melanoma. miR-944 was downregulated in melanoma cells, while SNHG6 silencing improved miR-944 level in A375 cells. Rescue experiments demonstrated that miR-944 overexpression reversed the effects of SNHG6 on A375 cell proliferation, migration and invasion. Altogether, SNHG6 exerted oncogenic effects in melanoma cells, providing a novel promising target for the treatment of melanoma.

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