SNHG11 contributes to NSCLC cell growth and migration by targeting miR-485-5p/BSG axis - 18/06/20
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Graphical abstract |
Highlights |
• | SNHG11 was overexpressed in NSCLC cells and promoted NSCLC cell growth and migration. |
• | SNHG11 acted as miR-485-5p sponge in NSCLC. |
• | BSG was a target gene of miR-485-5p and played an oncogenic role in NSCLC. |
• | SNHG11/miR-485-5p/BSG axis contributed to NSCLC cell growth and migration. |
Abstract |
Accumulating studies implied that long noncoding RNAs (lncRNAs) act as essential factors in regulating diverse biological behaviors of cancers. Small nucleolar RNA host gene 11 (SNHG11) has been reported as for its oncogenic properties in several cancer types. However, it is unclear whether SNHG11 exerts functions in non-small cell lung cancer (NSCLC) remains unclear. The aim of this study was to inspect the role and regulatory mechanism of SNHG11 in NSCLC. The expression of SNHG11 in NSCLC cells was analyzed by qRT-PCR. Functional experiments were carried out to determine the effects of SNHG11 silence on the biological behaviors of NSCLC cells, including growth, migration and epithelial-mesenchymal transition. The inhibition of above functions was observed after SNHG11 was silenced. Subcellular fractionation and FISH assays were performed to detect the cellular distribution of SNHG11. Moreover, SNHG11 was found to be a sponge of miR-485-5p that could directly target to Basigin (BSG) mRNA. The interaction between SNHG11 and miR-485-5p as well as between miR-485-5p and BSG was proven by RNA pull down and luciferase reporter assays. Restoration assay confirmed the involvement of miR-485-5p and BSG in SNHG11-mediated NSCLC cellular functions. Conclusively, SNHG11 was overexpressed in NSCLC and functioned as a miR-485-5p sponge to up-regulate BSG.
Le texte complet de cet article est disponible en PDF.Keywords : SNHG11, miR-485-5p, BSG, NSCLC
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