Knockdown of SNORA47 Inhibits the Tumorigenesis of NSCLC via Mediation of PI3K/Akt Signaling Pathway.

Huiqing Yu,Juan Gong,Sixiong Wang,Liejun Yang,Ling Tian,Shihong Liu

doi:10.3389/fonc.2021.620213

Huiqing Yu, Juan Gong + Show 4 more

Open Access

https://doi.org/10.3389/fonc.2021.620213

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Abstract

BackgroundNon-small cell lung cancer (NSCLC) is a frequently diagnosed aggressive cancer all over the world. Small nucleolar RNAs (snoRNAs) are a group of non-coding mediatory RNAs. A previous report indicated that small nucleolar RNA 47 (SNORA47) is upregulated in NSCLC. However, the role of SNORA47 in NSCLC is unclear.Material and MethodsCell proliferation was measured by immunofluorescence staining. Cell apoptosis and cycle of NSCLC were tested by flow cytometry and the protein expressions were investigated by Western-blot. Meanwhile, cell migration and invasion were detected by transwell assay. Xenograft mice model was established to detect the effect of SNORA47 knockdown on tumor growth of NSLC in vivo.ResultsKnockdown of SNORA47 significantly inhibited the proliferation of NSCLC cells via inducing cell apoptosis. Moreover, migration and invasion of NSCLC cells were notably decreased by SNORA47 shRNA. SNORA47 knockdown significantly induced G1 arrest in NSCLC cells via regulation of p27 Kip1, CDK2, and cyclin D1. Meanwhile, SNORA47 shRNA inhibited EMT process and PI3K/Akt signaling in NSCLC cells. Finally, silencing of SNORA47 significantly inhibited the tumor growth of NSCLC in vivo.ConclusionKnockdown of SNORA47 significantly inhibited the tumorigenesis of NSCLC via inhibition of PI3K/Akt signaling and EMT process. Thereby, our finding might shed a new light on exploring the strategies for the treatment of NSCLC.

Highlights

Non-small cell lung cancer (NSCLC) is the most frequent type of lung cancer which is known as the leading cause of cancer-associated death all over the world [1]
Zheng D et al found that SNORA78 could promote the tumorigenesis of NSCLC in vitro and in vivo [7]
Cell viability of NSCLC or BEAS-2B was notably decreased by small nucleolar RNA 47 (SNORA47) knockdown (Figure 1B and Supplementary Figure 1B), and SNORA47 shRNA1 significantly inhibited the proliferation of NSCLC or BEAS-2B cells (Figures 1C, D and Supplementary Figure 1C)

Summary

Introduction

Non-small cell lung cancer (NSCLC) is the most frequent type of lung cancer which is known as the leading cause of cancer-associated death all over the world [1]. Small nucleolar RNAs (snoRNAs) are a group of non-coding mediatory RNAs about the length of 60–300 nucleotides which are located in nucleolus of cells [4]. Mei YP et al indicated that SNORA42 could act as an oncogene in NSCLC [8]. The role of SNORA47 in NSCLC remains unclear. Non-small cell lung cancer (NSCLC) is a frequently diagnosed aggressive cancer all over the world. Small nucleolar RNAs (snoRNAs) are a group of non-coding mediatory RNAs. A previous report indicated that small nucleolar RNA 47 (SNORA47) is upregulated in NSCLC.

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Results

Conclusion