Abstract
Background: Long non-coding RNAs (lncRNAs) possess pivotal roles in human cancers, including thyroid cancer. In this study, we sought to elucidate the precise action of MIR31HG in the functional behaviors of thyroid cancer cells.Methods: MIR31HG, microRNA (miR)-761 and mitogen-activated protein kinase 1 (MAPK1) were quantified by quantitative real-time PCR (qRT-PCR) or immunoblotting analysis. Cell viability, proliferation, apoptosis, invasion, and migration abilities were evaluated by MTS, 5-Ethynyl-2’-Deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays, respectively. Dual-luciferase reporter assays were performed to validate the relationship between miR-761 and MIR31HG or MAPK1. Mouse xenografts were formed to assess the effect of MIR31HG on tumor growth.Results: MIR31HG expression was at high levels in thyroid cancer. Suppression of MIR31HG impeded cell proliferation, invasion, and migration, as well as promoted cell apoptosis in vitro, and diminished the growth of xenograft tumors in vivo. Mechanistically, MIR31HG targeted and regulated miR-761. Moreover, the effects of MIR31HG suppression was partly dependent on increased abundance of miR-761. MAPK1 was established as a direct and functional target of miR-761. Furthermore, MIR31HG involved the modulation of MAPK1 expression through competitively binding to miR-761 by the shared binding sequence.Conclusion: Our findings demonstrate the workings of an undescribed regulatory network, in which MIR31HG targets miR-761 to regulate MAPK1 expression, leading to the alteration of the functional behaviors of thyroid cancer cells.
Long Non-Coding RNA MAPK8IP1P2 Inhibits Lymphatic Metastasis of Thyroid Cancer by Activating Hippo Signaling via Sponging miR-146b-3p
