SPI1-induced upregulation of lncRNA SNHG6 promotes non-small cell lung cancer via miR-485-3p/VPS45 axis.

More and more researches have proved that long noncoding RNAs (lncRNAs) are vital regulators and biological participants in human cancers [1-5]. SnoRNA host gene 6 (SNHG6) was found to have an effect on the early stage and tumorigenesis in many cancers [6-10]. However, the expression of SNHG6 and its role of in non-small cell lung cancer (NSCLC) still need to be investigated. This work aims to investigate the expression and its biological role in NSCLC. In our study, the expression of SNHG6 was abnormally high in NSCLC tissues and cells. The negative impact of SNHG6 expression on the overall survival of patients with NSCLC was analyzed with Kaplan Meier method. Functionally, loss of SNHG6 expression led to the inhibition on the growth, migration and invasion of NSCLC cells. Mechanistically, miR-485-3p was necessary for the regulatory relation between SNHG6 and VPS45. More importantly, SPI1 could promote the expression of SNHG6 via transcriptionally activation. In conclusion, we proved that SPI1/SNHG6/miR-485-3p/VPS45 axis exerted oncogenic role in the cellular process of NSCLC cells.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}