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. 2019 Jan 30;10(5):1333-1340.
doi: 10.7150/jca.29517. eCollection 2019.

Knockdown of long non-coding RNA SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway

Xuanhao Hu  1 , Yang Hong  2 , Chao Shang  1
Affiliations
Free PMC article

Knockdown of long non-coding RNA SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway

Xuanhao Hu et al. J Cancer. .
Free PMC article

Abstract

Objective: Human brain glioma is the most malignant primary intracranial tumor, which has poor prognosis and high mortality. Long noncoding RNAs are considered to take part in cellular phenotypes and are emerging as diagnostic and prognostic biomarkers of glioma. This study will research the effects of Small Nucleolar RNA Host Gene 5 (SNHG5) gene on malignant cellular phenotypes in glioma and explore the possible mechanisms. Materials and Methods: The expression level of SNHG5 was examined using quantitative Real-time PCR in glioma tissues and cell lines. Loss-of-function experiments of SNHG5 together with Enhanced Cell Counting Kit-8, flow cytometry and cell invasion assay were used to investigate the effects of SNHG5 on malignant cellular phenotypes of glioma cells. Finally, luciferase assay and western blotting were applied to determine the activity of WNT/CTNNB1 signaling pathway. Results: SNHG5 gene was high-expressed in glioma tissues and cell lines. Knockdown of SNHG5 gene depressed cell proliferation and invasiveness as well as promoted the apoptosis of U251 and U87 cells. In addition, online database analysis showed SNHG5 was closely related to Wnt/CTNNB1 signaling pathway. Knockdown of SNHG5 inactivated Wnt/CTNNB1 signaling pathway, and the activating of Wnt/CTNNB1 signaling pathway partly restored the influences of SNHG5 knockdown on malignant cellular phenotypes of U251 and U87 cells. Conclusion: SNHG5 gene was high-expressed in glioma, knockdown of SNHG5 inhibits malignant cellular phenotypes of glioma via Wnt/CTNNB1 signaling pathway.

Keywords: Long non-coding RNA; Small Nucleolar RNA Host Gene 5; Wnt/CTNNB1 signaling pathway; glioma; malignant cellular phenotypes.

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Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

Figures

Figure 1
Figure 1
SNHG5 was high-expressed in glioma tissues and cell lines. A: Representative microarray analysis of SNHG5 in glioma and NBT specimens. B: The expression levels of SNHG5 in glioma specimens and NBT specimens. ** P<0.01 vs NBT group. C: The expression levels of SNHG5 in NHA, U251 and U87 cell lines. ** P<0.01 vs NHA group.
Figure 2
Figure 2
Knockdown of SNHG5 inhibited malignant cellular phenotypes of glioma cells. A: The expression levels of SNHG5 in U251 and U87 cells. B: The cell proliferation of U251 and U87 cells. C: The cell invasiveness of U251 and U87 cells. D: The cell apoptosis rate of U251 and U87 cells. ** P<0.01 vs sh-NC group.
Figure 3
Figure 3
Knockdown of SNHG5 inactivated Wnt/CTNNB1 signaling pathway. A: The co-expression patterns between SNHG5 and GSK3B in TCGA Pan-Cancer (PANCAN) database with 171 glioma samples. B: The co-expression patterns between SNHG5 and CTNNB1 in TCGA Pan-Cancer (PANCAN) database with 171 glioma samples. C: The ratio of TOP/FOP luciferase values in U251 and U87 cells. D: The expression of GSK3B and CTNNB1 protein in U251 and U87 cells. ** P<0.01 vs sh-NC group.
Figure 4
Figure 4
Knockdown of SNHG5 inhibited malignant cellular phenotypes of glioma cells via Wnt/CTNNB1 signaling pathway. A: The ratio of TOP/FOP luciferase values in U251 and U87 cells. B: The expression of CTNNB1 protein in U251 and U87 cells. C: The cell proliferation of U251 and U87 cells. D: The cell invasiveness of U251 and U87 cells. E: The cell apoptosis rate of U251 and U87 cells. ** P<0.01 vs sh-NC + pE-NC group, ## P<0.01 vs sh-SNHG5 + pE-NC group.
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