The number of thyroid cancer (THCA) cases has increased dramatically worldwide. Many previous reports have confirmed that lncRNA is involved in the pathogenesis of THCA. However, the role and mechanism of lncRNA RUNDC3A-AS1 in THCA have not been studied. We intended to explore the effect of RUNDC3A-AS1 on the proliferation and apoptosis of THCA cells. Relative expression levels of RUNDC3A-AS1, microRNA (miR)-151b, and small nuclear ribonucleoprotein polypeptides B and B1 (SNRPB) were examined by reverse transcription quantitative polymerase chain reaction (RT-qPCR) in THCA cells. The localization of RUNDC3A-AS1 in THCA cells was detected by subcellular fractionation assay. The cell proliferation was tested by 5-ethynyl-2'-deoxyuridine (EdU), cell counting kit-8 (CCK-8), and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Flow cytometry was used to examine the cell apoptosis capacity. The relationships between RUNDC3A-AS1 and miR-151b or miR-151b and SNRPB were verified by luciferase reporter assay. The protein level was detected by Western blot analysis. RUNDC3A-AS1 exhibited high expression in THCA cells. RUNDC3A-AS1 knockdown suppressed cell proliferation but induced cell apoptosis. Importantly, RUNDC3A-AS1 targeted miR-151b to regulate the SNRPB expression. In rescue assays, SNRPB overexpression partially reversed the suppressive effect of RUNDC3A-AS1 knockdown on cell proliferation and the promotive effect of RUNDC3A-AS1 knockdown on cell apoptosis. The RUNDC3A-AS1/miR-151b/SNRPB axis regulated THCA cell proliferation and apoptosis, which provides novel insight into THCA investigation at the molecular level.
Copyright © 2022 Yan Deng et al.