Introduction: Follicular thyroid carcinoma (FTC) is more aggressive than the most common papillary thyroid carcinoma (PTC). However, the current research on FTC is less than PTC. Here, we investigated the effects of long noncoding RNA (lncRNA) GAS5 and miR-221-3p in FTC. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect GAS5 and miR-221-3p expression in the FTC tissues and cells. Cell proliferation was assessed by CCK8 and EdU assays. Flow cytometry was performed to determine the cell cycle. The dual-luciferase reporter assay was employed to validate the binding relationship of GAS5/miR-221-3p and miR-221-3p/cyclin-dependent kinase inhibitor 2B (CDKN2B). Western blot was conducted to measure the protein level of CDKN2B. Results: Our results displayed that GAS5 was downregulated, while miR-221-3p was upregulated in FTC tissues and cells. What’s more, overexpression of GAS5 or miR-221-3p inhibition induced G0/G1 phase arrest and inhibited cell proliferation of FTC cells. GAS5 acted as a sponge of miR-221-3p, and CDKN2B was a target gene of miR-221-3p. Additionally, GAS5 inhibited cell cycle and proliferation of FTC cells via reducing miR-221-3p expression to enhance CDKN2B expression. Conclusion: GAS5 induced G0/G1 phase arrest and inhibited cell proliferation via targeting miR-221-3p/CDKN2B axis in FTC. Thus, GAS5 may be a potential therapeutic target for the treatment of FTC.
Pathobiology

中文翻译：

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长链非编码 RNA GAS5 靶向 miR-221-3p/细胞周期蛋白依赖性激酶抑制剂 2B 轴调节滤泡性甲状腺癌细胞周期和增殖

简介：滤泡性甲状腺癌 (FTC) 比最常见的甲状腺乳头状癌 (PTC) 更具侵袭性。但是，目前对FTC的研究还少于PTC。在这里，我们研究了长链非编码 RNA (lncRNA) GAS5 和 miR-221-3p 在 FTC 中的影响。方法：采用定量实时聚合酶链反应（qRT-PCR）检测 FTC 组织和细胞中 GAS5 和 miR-221-3p 的表达。通过 CCK8 和 EdU 测定评估细胞增殖。进行流式细胞术以确定细胞周期。双荧光素酶报告基因检测用于验证 GAS5/miR-221-3p 和 miR-221-3p/细胞周期蛋白依赖性激酶抑制剂 2B (CDKN2B) 的结合关系。进行蛋白质印迹以测量CDKN2B的蛋白质水平。结果：我们的结果显示 GAS5 被下调，而 miR-221-3p 在 FTC 组织和细胞中被上调。此外，过表达 GAS5 或 miR-221-3p 抑制诱导 G0/G1 期停滞并抑制 FTC 细胞的细胞增殖。GAS5充当miR-221-3p的海绵，CDKN2B是miR-221-3p的靶基因。此外，GAS5 通过降低 miR-221-3p 表达来增强 CDKN2B 表达来抑制 FTC 细胞的细胞周期和增殖。结论： GAS5通过靶向FTC中的miR-221-3p/CDKN2B轴诱导G0/G1期阻滞并抑制细胞增殖。因此，GAS5 可能是治疗 FTC 的潜在治疗靶点。
病理生物学