MiR-630 inhibits papillary thyroid carcinoma cell growth, metastasis, and epithelial-mesenchymal transition by suppressing JAK2/STAT3 signaling pathway

X.-M. Pan, X.-Y. He, Y.-L. Yang, W.-J. Jia, Z.-Q. Yang, D. Yan, J.-X. Ma

Department of General Surgery, Gansu Provincial Hospital, Lanzhou, Gansu, China. jshfees6372@sohu.com

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• Oncology

OBJECTIVE: Evidence has demonstrated that miR-630 is involved in multiple processes in cancer development and progression. However, the exact functions of miR-630 in papillary thyroid carcinoma (PTC) and the underlying mechanisms remain undefined. Therefore, the aims of the present study were to investigate the role and potential mechanism of miR-630 in tumorigenicity of PTC.

PATIENTS AND METHODS: Microarrays were used to analyze the differentially expressed miRNAs in PTC tissues. Expression of miR-630 in PTC tissues and cell lines were determined by a qRT-PCR assay. CCK-8 assays, clonogenic survival assays, cell apoptosis analysis, wound healing assays and transwell invasion assays were used to examine the tumorigenesis function of miR-630 in vitro. Protein expression of signaling pathways was determined by using Western blot.

RESULTS: We found that miR-630 was significantly downregulated in PTC tissues and cell lines. Overexpression of miR-630 inhibited PTC cell proliferation and induced cell apoptosis via suppressing the expression of caspase-3 and caspase-6. In addition, up-regulation of miR-630 suppressed the migration and invasion in PTC cells by suppressing EMT progress. Mechanistic investigations showed forced miR-660 expression decreased proteins expression of phosphorylation levels in JAK2/STAT3 signaling.

CONCLUSIONS: We firstly provided the evidence that miR-630 displayed a tumor-promotive role in PTC progression through modulating JAK2/STAT3 pathway, and that a potential therapeutic strategy through enhancing miR-630 expression might benefit PTC patients.

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