Abstract

BackgroundBreast cancer (BC) is a malignant tumor that occurs in the epithelial tissue of the breast gland. Long non-coding RNA (lncRNA) small nucleolar RNA host gene 3 (SNHG3) has been found to promote BC cell proliferation and invasion by regulating the microRNA (miR)-101/zinc-finger enhancer binding axis in BC. Herein, the objective of the present study is to evaluate the effect of lncRNA SNHG3 on BC cell proliferation and metastasis with the Notch signaling pathway.MethodsDifferentially expressed lncRNA in BC tissues and normal breast tissues was analyzed. SNHG3 si-RNA-1 and SNHG3 si-RNA-2 were constructed to detect the mechanism of SNHG3 interference in BC cell proliferation, viability, migration and invasion. Then, dual-luciferase reporter gene assay was utilized to verify the binding relation between SNHG3 and miR-154-3p as well as miR-154-3p and Notch2. Moreover, xenograft transplantation was applied to confirm the in vitro experiments.ResultsHighly expressed SNHG3 was observed in BC tissues. The growth of BC cells in vivo and in vitro was evidently repressed after silencing SNHG3. BC cell invasion and migration were inhibited by silencing SNHG3 in vitro. SNHG3 could act as a competing endogenous RNA of miR-154-3p and upregulate the Notch signaling pathway to promote BC cell development. Activation of the Notch signaling pathway can partly reverse the inhibition of cell activity induced by silencing SNHG3.ConclusionOur study demonstrated that interfered lncRNA SNHG3 promoted BC cell proliferation and metastasis by activating the Notch signaling pathway. This investigation may offer new insight for BC treatment.

Highlights

  • Breast cancer (BC) is a malignant tumor that occurs in the epithelial tissue of the breast gland

  • LncRNA small nucleolar RNA host gene 3 (SNHG3) was highly expressed in BC patients Firstly, the expression difference of Long non-coding RNA (lncRNA) between BC tissues and normal breast tissues were detected by transcriptome sequencing

  • Liu L. et al have suggested that lncRNA SNHG3 existed as an oncogene in lung adenocarcinoma, and upregulation of lncRNA SNHG3 promoted lung adenocarcinoma cell growth [22]

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Summary

Introduction

Breast cancer (BC) is a malignant tumor that occurs in the epithelial tissue of the breast gland. The objective of the present study is to evaluate the effect of lncRNA SNHG3 on BC cell proliferation and metastasis with the Notch signaling pathway. It remains challenging to ascertain an individual basis who would benefit from these treatments while who would be possible to encounter toxicities [4]. In this context, novel therapeutic strategies for BC are in urgent need. We undertook a long noncoding RNA (lncRNA)-based approach to understand the underlying mechanism in BC development, in order to develop novel intervention strategies

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