Knockdown of lncRNA SNHG16 suppresses multiple myeloma cell proliferation by sponging miR-342-3p

Xi Yang,Hong Liu,Xinfeng Wang,Haiyan Liu,Hongming Huang,Zenghua Lin

doi:10.1186/s12935-020-1118-1

Abstract

BackgroundAberrant expression of long non-coding RNAs (lncRNAs) is closely associated with development and prognosis of human cancers. LncRNA SNHG16 is reportedly involved in human cancer; however, its roles in multiple myeloma (MM) remain unclear.MethodsIn this study, we investigated the function and molecular mechanisms of SNHG16 in MM. MM cells were transfected with si-SNHG16 or si-NC. SNHG16 expression levels was measured by qRT-PCR. Cell proliferation was monitored using the MTS. Flow cytometry assay was performed to measure the cell cycle and apoptosis. Luciferase reporter assay were performed to confirm the sponged miRNAs of SNHG16.ResultsSNHG16 expression was up-regulated in MM tissues. SNHG16 knockdown suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted the apoptosis of MM cells. Moreover, SNHG16 knockdown promoted cleaved-Caspase-3, cleaved-Caspase-9, Foxa3a, and Bax expression, while markedly inhibiting CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. miR-342-3p was a direct target of SNHG16. SNHG16 knockdown significantly increased miR-342-3p expression in MM cells. Overexpression miR-342-3p markedly suppressed cell proliferation, arrested cell cycle transition from G1 to S phase, and promoted apoptosis of MM cells. Overexpression of miR-342-3p markedly promoted cleaved-Caspase-3/-9, Foxa3a, and Bax expression, and inhibited CCND1, Bcl-2, Cyclin D1, PI3K, and p-AKT expression in MM cells. Additionally, repression of miR-342-3p could rescue the effect of SNHG16 knockdown on MM cell proliferation, cycle arrest, apoptosis, and related protein expression.ConclusionKnockdown of lncRNA SNHG16 suppresses MM cell proliferation by sponging miR-342-3p, implicating SNHG16 as a novel therapeutic target for MM.

Highlights

Aberrant expression of long non-coding RNAs is closely associated with development and prognosis of human cancers
Small Nucleolar RNA Host Gene 16 (SNHG16) is significantly up‐regulated in MM samples and MM cells First, we found that SNHG16 expression was significantly up-regulated in MM patients compared with that in controls (Fig. 1a)
SNHG16 knockdown significantly suppressed cell proliferation (Fig. 2b, c), arrested cell cycle transition from the G1 to S phase (Fig. 2d), and promoted cell apoptosis (Fig. 3a, b) both in RPMI-8226 and NCI-H929 cells compared with corresponding negative control

Summary

Introduction

Aberrant expression of long non-coding RNAs (lncRNAs) is closely associated with development and prognosis of human cancers. LncRNA SNHG16 is reportedly involved in human cancer; its roles in multiple myeloma (MM) remain unclear. Multiple myeloma (MM) is a fatal plasmocyte malignancy [1]. Increasing evidence indicates that the aberrant expression of long non-coding RNAs (lncRNAs) are closely associated with the development and prognosis of. Yang et al Cancer Cell Int (2020) 20:38 various types of cancer, including MM [5]. LncRNA Small Nucleolar RNA Host Gene 16 (SNHG16), an SNHG member, is up-regulated and functions as an oncogene in pancreatic cancer [7] and gastric cancer [8]. SNHG16 plays important roles in different cancers, its functional role and underlying molecular mechanism in MM tumorigenesis are still largely unclear

Objectives

Methods

Results

Discussion

Conclusion