SNHG8 is identified as a key regulator in non-small-cell lung cancer progression sponging to miR-542-3p by targeting CCND1/CDK6

Abstract

BackgroundRecently, various dynamically expressed lncRNAs are known to play critical roles in cancer progression. Small nucleolar RNA host genes (SNHG), a stable cytoplasmic lncRNA, which have been widely reported to act as an oncogene in non-small cell lung cancer (NSCLC). As an important member of SNHG, SNHG8 have been suggested to over-expressed in several cancer disease, while the biological function in NSCLC remains unclear.PurposeHere we investigated the biological function and underlying mechanism of SNHG8 in human NSCLC.Patients and methodsThe relationship between SNHG8 expression and clinicopathologic characteristic in NSCLC patients were observed from January 2014 to December 2014 in 120 NSCLC patients. The expression of SNHG8 were analyzed by qRT-PCR assay in cancer tissues and cells. Cell proliferation ability were detected in NSCLC cells by CCK-8 assay. Flow cytometric analysis were performed to detected the cell apoptosis and cell cycle. Luciferase assay and Western blot assay were performed on NSCLC cells to detected the underlying mechanism of SNHG8 in NSCLC. Moreover, Tumor xenografts in nude mice were performed to detected the in vivo function of SNHG8.ResultsSNHG8 was over-expressed in NSCLC tissues and cells. Patients with high SNHG8 expression have poorer overall survival (OS) and progression-free survival (PFS) than the patients with low SNHG8 expression. SNHG8 knockdown inhibited NSCLC cell proliferation in vitro and in vivo, arrested cell cycle in the G0/G1 phase via targeting miR-542-3p/CCND1/ CDK6, and induced cell apoptosis via activation of Caspase-3.ConclusionSNHG8 negatively regulated miR-542-3p in NSCLC progression by regulating downstream effectors including CCND1 and CDK6. SNHG8 showed great potential for the application in the treatment of NSCLC.

The prognostic value of lncRNA SNHG4 and its potential mechanism in liver cancer

“…Recently, many studies have found that the aberrant expression of snoRNAs might act as an oncogene in the progression of the tumor. For example, Chen found that SNHG8 overexpressed in non-small cell lung carcinoma (NSCLC) [32], and Dong found that SNHG8 is an oncogene in human hepatocellular carcinoma [33], Meng found SNHG6 promotes glioma tumorigenesis in glioma [34], and Zhu found SNHG4 overexpressed in hepatocellular carcinoma [35]. Consistent with these studies, we found higher SNHG4 expression in liver cancer and it may be a biomarker.…”

<p>SNHG8 is upregulated in esophageal squamous cell carcinoma and directly sponges microRNA-411 to increase oncogenicity by upregulating KPNA2</p>

“…25 Furthermore, SNHG8 is overexpressed in non-small cell lung cancer tissues and cell lines. 26 Patients with non-small cell lung cancer overexpressing SNHG8 show shorter overall survival and shorter progression-free survival relative to the patients with low SNHG8 expression. 26 However, the expression profile and clinical value of SNHG8 in ESCC have remained elusive and merit research.…”

“…26 Patients with non-small cell lung cancer overexpressing SNHG8 show shorter overall survival and shorter progression-free survival relative to the patients with low SNHG8 expression. 26 However, the expression profile and clinical value of SNHG8 in ESCC have remained elusive and merit research. In this study, we found that SNHG8 expression is high in ESCC tissues and cell lines.…”

“…Many recent studies indicate that SNHG8 is overexpressed in multiple types of human cancer, [24][25][26] suggesting that this lncRNA may promote the aggressiveness of these cancers. However, whether SNHG8 is aberrantly expressed in ESCC and its biological functions have yet to be elucidated.…”

LncRNA SNHG8 accelerates proliferation and inhibits apoptosis in HPV‐induced cervical cancer through recruiting EZH2 to epigenetically silence RECK expression

“…Herein, SNHG8, was agreed as a potent multiple tumor facilitator in previous research. [15][16][17][18][19] One thing we have in common with previous studies was that SNHG8 was upregulated and aggravated tumorigenesis. However, the stimulating effect of SNHG8 in HPV-positive CC cells was first disclosed in the present study.…”