Circular RNA DOCK1 downregulates microRNA‐124 to induce the growth of human thyroid cancer cell lines

波形蛋白 细胞周期蛋白D1 癌症研究 甲状腺癌 下调和上调 免疫印迹 癌变 活力测定 小RNA 化学 癌症 生物 甲状腺 细胞 医学 细胞周期 内科学 免疫学 内分泌学 免疫组织化学 生物化学 基因
作者
Wei Cui,Jun Xue
出处
期刊:Biofactors [Wiley]
卷期号:46 (4): 591-599 被引量:35
标识
DOI:10.1002/biof.1662
摘要

Abstract Background Both circular RNA DOCK1 (circDOCK1) and microRNA‐124 (miR‐124) are implicated in carcinogenesis, but functional association between these two molecules remains uncharacterized. Here, we aimed to ascertain the role of circDOCK1‐miR‐124 node in thyroid cancer cells. Methods circDOCK1 in thyroid cancer specimens from 25 patients was quantified by qRT‐PCR. FTC‐133 and TPC‐1 cells were enforced to overproduce circDOCK1 and miR‐124 which were confirmed by qRT‐PCR. The alteration in viability, migration and invasion was monitored. Cellular lysis was subjected to Western blot for detecting cyclin D1, p53, matrix metallopeptidase 9 (MMP‐9), and vimentin. The phosphorylation of JAK1, STAT3, and AMPK was determined by Western blot. Results Results from qRT‐PCR showed circDOCK1 was enriched in thyroid carcinoma tissues. circDOCK1 fortified the viability of FTC‐133 and TPC‐1 cells, as well as their activities to migrate and invade. circDOCK1 increased cyclin D1 and decreased p53, and meanwhile induced the accumulation of MMP‐9 and vimentin. miR‐124 conferred a reverse effect on the abovementioned alteration. Besides, miR‐124 blockaded the phosphorylation of JAK1, STAT3, and AMPK which was induced by circDOCK1. Conclusion circDOCK1 contributed to thyroid carcinogenesis through inhibition of miR‐124 in thyroid cancer cells with dampening signaling transduction of JAK/STAT/AMPK in virtue of miR‐124 downregulation.
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