Effect of miR-206 over-expression on proliferation and migration of pap?illary thyroid carcinoma K1 cells |
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Authors: | DU Xi-feng HU Zhi-hui JING Min-jie WANG Ya-ting LAN Li-zhen |
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Institution: | Department of Endocrinology, The First Hospital of Shanxi Medical University, Taiyuan 030001, China. |
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Abstract: | AIMTo determine the effect of microRNA-206 (miR-206) on proliferation and migration of human papillary thyroid carcinoma K1 cells and to explore its possible mechanism. METHODSThe expression of miR-206 in the K1 cells was detected by RT-qPCR. The cell viability was detected by CCK-8 assay. The number of viable K1 cells was counted by the method of Trypan blue exclusion. The migration ability of K1 cells was detected by Transwell chamber migration assay. Bioinformatics software was used to predict the target gene of miR-206. The targeting relationship between miR-206 and c-Met was verified by dual-luciferase reporter assay. The protein levels of c-Met, p-Met, AKT, p-AKT, mTOR and p-mTOR were determined by Western blot. RESULTSAfter the K1 cells were transfected with miR-206 mimic transiently, the relative expression of miR-206 in treatment group was significantly higher than that in blank group and negative control group (P<0.01). The results of CCK-8 assay and Trypan blue exclusion assay showed that the proliferation ability of K1 cells in treatment group transfected with miR-206 mimic was significantly inhibited compared with other groups (P<0.01). The results of Transwell assay showed that the number of migratory K1 cells in treatment group was lower than that in blank group and negative control group (P<0.01). Moreover, our results demonstrated that miR-206 directly targeted c-Met and repressed the activation of downstream AKT/mTOR signaling pathway. CONCLUSION miR-206 over-expression inhibits the proliferation and migration abilities of papillary thyroid carcinoma K1 cells, and its mechanism may be related to the inhibition of c-Met/AKT/mTOR signaling pathway. |
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Keywords: | MicroRNA-206 Papillary thyroid carcinoma Cell proliferation Cell migration c-Met/AKT/mTOR signaling pathway |
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