Long non-coding RNA HOTAIR promotes cell viability, migration and invasion in thyroid cancer cells by sponging miR-17-5p.

Thyroid cancer is a common endocrine malignancy. Long non-coding RNAs (lncRNAs) were reported to regulate cellular processes in tumorigenesis and development. In this study, we mainly investigated the role of Homeobox Transcript Antisense Intergenic RNA (HOTAIR) in thyroid cancer and its potential mechanism. RT-qPCR was conducted to evaluate the expression of HOTAIR and miR-17-5p in thyroid cancer tissues and 4 cell lines (TPC-1, FTC-133, B-CPAP and SW579). MTT assay was employed to analyze the cell viability of TPC-1 and FTC-133 cells. The migration and invasion of TPC-1 and FTC-133 cells were detected via Transwell assay. Luciferase reporter assay was used to validate the target of HOTAIR. In vivo tumor formation assay in nude mice was applied to investigate the impact of HOTAIR on thyroid cancer tumorigenesis. HOTAIR was significantly upregulated, while miR-17-5p was downregulated in thyroid cancer tissues and cells, and the miR-17-5p expression in thyroid cancer tissues was inversely correlated with HOTAIR expression. Silencing HOTAIR significantly inhibited the cell viability, migration and invasion of TPC-1 and FTC-133 cells. MiR-17-5p was a target of HOTAIR and counter-regulated by HOTAIR. Introduction of miR-17-5p also inhibited the cell viability, migration and invasion in TPC-1 and FTC-133 cells. Moreover, introduction of miR-17-5p reversed knockdown of HOTAIR-mediated the suppression effects on the cell viability, migration and invasion in thyroid cancer cells. Additionally, knockdown of HOTAIR inhibited thyroid cancer tumorigenesis in mice. Our results suggested HOTAIR promotes cell viability, migration and invasion in thyroid cancer cells by sponging miR-17-5p.