miR-215 suppresses papillary thyroid cancer proliferation, migration, and invasion through the AKT/GSK-3β/Snail signaling by targeting ARFGEF1

Cell Death & Disease
Jihua HanJiewu Zhang

Abstract

The incidence of papillary thyroid cancer (PTC) has been rapidly increasing in recent years. PTC is prone to lymph node metastasization, which further increases the recurrence rate and mortality of thyroid cancer. However, the underlying mechanisms of this process remain elusive. Several reports have shown that the microRNA miR-215 plays an important role in cancer metastasis. Here, we investigated, for the first time, the potential association between miR-215 and metastasis in PTC. The results of qPCR analysis demonstrated that miR-215 was downregulated in PTC cell lines and tissues, and lower levels of miR-215 correlated with lymph node metastasis of PTC. In vitro and in vivo assays revealed that restoration of miR-215 dramatically inhibited PTC cell proliferation and metastasis. We identified ADP ribosylation factor guanine nucleotide-exchange factor 1 (ARFGEF1) as the target, which mediated the function of miR-215. The expression of ARFGEF1 was inhibited by miR-215, and the effects of miR-215 were abrogated by re-expression of ARFGEF1. Moreover, we found that miR-215 suppressed PTC metastasis by modulating the epithelial-mesenchymal transition via the AKT/GSK-3β/Snail signaling. In summary, our study proves that miR-215 inh...Continue Reading

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Citations

Jun 15, 2019·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Fu-I LuChun-Chun Li
Jul 17, 2020·Computational and Mathematical Methods in Medicine·Xinhua XuRongbiao Ying
Sep 7, 2020·World Journal of Surgical Oncology·Wan-Ping GuoWei Ma
Jun 3, 2021·Journal of Clinical Medicine·Katarzyna Wieczorek-Szukala, Andrzej Lewinski
Jul 21, 2021·Journal of Cardiovascular Pharmacology·Xiaojv XiongJijun Liu

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Methods Mentioned

BETA
transfection
xenografts
xenograft
PCR
electrophoresis
Assay

Software Mentioned

SPSS
Prism
GraphPad

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