Journal
BIOFACTORS
Volume 46, Issue 4, Pages 591-599Publisher
WILEY
DOI: 10.1002/biof.1662
Keywords
DOCK180; invasion; JAK; STAT; AMPK; migration; proliferation
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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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