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

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

JOURNAL=Frontiers in Oncology

VOLUME=11

YEAR=2021

URL=https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2021.620213

DOI=10.3389/fonc.2021.620213

ISSN=2234-943X

ABSTRACT=<sec><title>Background</title><p>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. However, the role of SNORA47 in NSCLC is unclear.</p></sec><sec><title>Material and Methods</title><p>Cell 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 <italic>in vivo</italic>.</p></sec><sec><title>Results</title><p>Knockdown of SNORA47 significantly inhibited the proliferation of NSCLC cells <italic>via</italic> 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 <italic>via</italic> 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 <italic>in vivo</italic>.</p></sec><sec><title>Conclusion</title><p>Knockdown of SNORA47 significantly inhibited the tumorigenesis of NSCLC <italic>via</italic> 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.</p></sec>