The purpose of this study was to explore the potential role of HOTAIR in thyroid cancer carcinogenesis. We found that HOTAIR was unregulated in human thyroid cancer and inversely correlated with miR-1. Functional assays indicated HOTAIR regulates miR-1 directly in thyroid cancer cells. We also revealed that HOTAIR promotes the processes of thyroid cancer cell malignancy through regulation of microRNA-1 (miR-1). Furthermore, we showed that HOTAIR could regulate a downstream target of miR-1, CCND2, in a miR-1-mediated manner. In addition, we also proved, using a tumor formation assay in nude mice, that silencing HOTAIR inhibited tumor formation . Therefore, our study demonstrated that HOTAIR promotes the development and progression of thyroid cancer through inhibition of microRNA-1 and activation of CCND2.
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