LncRNA SNHG4 promotes tumour growth by sponging miR-224-3p and predicts poor survival and recurrence in human osteosarcoma.

Abstract:

OBJECTIVE:Accumulating data show that dysregulation of long noncoding RNAs (lncRNAs) acts a critical role in a variety of malignancies. Among these lncRNAs, small nucleolar RNA host genes (SNHGs) are associated with tumour growth and progression. But, the molecular mechanisms by which SNHG4 contributes to osteosarcoma remain undocumented. METHODS:The association between lncRNA SNHG4 expression and clinicopathologic characteristics and prognosis in patients with osteosarcoma was analysed by TCGA RNA-sequencing data. Cell viability and colony formation abilities were respectively assessed by MTT and colony formation assays. LncRNA SNHG4-specific binding with miR-224-3p was verified by bioinformatic analysis, luciferase gene report, and RNA immunoprecipitation assays. Regulation relationship between SNHG4 and miR-224-3p expression was further evaluated by the rescue experiments. RESULTS:The expression level of lncRNA SNHG4 was significantly elevated in osteosarcoma samples and cell lines as compared with the adjacent normal tissues, and SNHG4 high expression was associated with tumour size (TS) and poor prognosis in patients with osteosarcoma. Knockdown of SNHG4 suppressed cell viability and invasive potential, whereas ectopic SNHG4 expression displayed the opposite effects. Moreover, we found that lncRNA SNHG4 acted as a sponge of miR-224-3p, and miR-224-3p mimic reversed SNHG4 induced tumour-promoting effects in osteosarcoma cells. The expression of miR-224-3p depicted a negative correlation with SNHG4 in osteosarcoma samples and miR-224-3p low expression was associated with TS and poor survival in patients with osteosarcoma. CONCLUSION:Our findings demonstrated that LncRNA SNHG4 promoted tumour growth by sponging miR-224-3p and represented a poor prognostic factor in patients with osteosarcoma.

journal_name

Cell Prolif

journal_title

Cell proliferation

authors

Xu R,Feng F,Yu X,Liu Z,Lao L

doi

10.1111/cpr.12515

subject

Has Abstract

pub_date

2018-12-01 00:00:00

pages

e12515

issue

6

eissn

0960-7722

issn

1365-2184

journal_volume

51

pub_type

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