NPSR1-AS1 activates the MAPK pathway to facilitate thyroid cancer cell malignant behaviors via recruiting ELAVL1 to stabilize NPSR1 mRNA

Abstract

ABSTRACT Thyroid cancer (TC) is a prevailing malignant disease in endocrine system. Recent reports have demonstrated that long non-coding RNAs (lncRNAs) are crucial participators in TC progression. In our study, we majorly investigated the molecular mechanism of neuropeptide S receptor 1 antisense RNA 1 (NPSR1-AS1) in TC. Western blot and qPCR analyses were applied for the measurement of protein and RNA expressions in TC cells. Colony formation, EdU, and transwell assays, supported by western blot analyses, were implemented for probing NPSR1-AS1 impacts on TC cell malignant phenotype. Moreover, bioinformatics prediction, RIP and Actinomycin D assays detected the downstream mechanism of NPSR1-AS1 in TC cells. In short, NPSR1-AS1 displayed high expression TC cells, and NPSR1-AS1 silence inhibited TC cell malignant behaviors. Additionally, NPSR1-AS1 positively regulated its nearby gene neuropeptide S receptor 1 (NPSR1). ELAV like RNA binding protein 1 (ELAVL1) served as the RNA-binding protein (RBP) to combine with NPSR1-AS1 and NPSR1. Silencing of ELAVL1 reduced the stability of NPSR1 mRNA. Moreover, NPSR1 could activate the mitogen-activated protein kinases (MAPK) pathway in TC cells. Collectively, our study elucidated the aspect of lncRNA-RBP-mRNA interaction which might be a novel sight for TC treatment.