| Objective:Iodine can affect the occurrence and development of papillary thyroid carcinoma,but the mechanism remains unclear.Micro RNA200c(miR-200c)is involved in tumorigenesis and development of multiple tumors.However,its role in iodine-induced thyroid cancer remains unclear.The objective of this study was to investigate the pathways associated with miR-200 c and the role of iodine in papillary thyroid carcinoma.The study aimed to provide a basis for further study of the effect of iodine on the pathogenesis of papillary thyroid carcinoma.Method:We employed RT-qpcr to detect the expression of miR-200 c in Nthy-ori 3-1 cell line(human normal thyroid cell)and TPC-1 cells line(human papillary thyroid carcinoma cell)respectively and changes of miR-200 c expression levels in Nthy-ori 3-1 cell line and TPC-1 cell lines treated with different concentrations of KI for 48 h.Western blot was utilized to detect the expression of YAHAG of the papillary thyroid carcinoma cell line after treated with different KI concentrations for 48 h and effects of up/downregulation of miR-200 c on the expression of YWHAG.CCK8 method and scratch assay experiment were used to detect the impacts of different concentrations of KI solution and up/downregulation of miR-200 c on the proliferation and migration of TPC-1 cells.Results:1.The results of RT-qpcr suggested that the expression of miR-200 c was lower in the TPC-1 cell line of compared with the Nthy-ori 3-1 cell line(P<0.01)2.The two groups of cells were treated with different concentrations of KI at 0μM,25μM,50μM and 75μM for 48 h,the expression of miR-200 c in the Nthy-ori 3-1 cell line was not statistically different,and the expression of miR-200 c in the 50μM and 75μM treatment groups of TPC-1was significantly upregulated compared with the 0um treatment group,which was statistically significant(P<0.01).However,the expression of miR-200 c in the 25μM treatment group of TPC-1 was not significantly different from that in the 0μM treatment group.3.The results of RT-q PCR suggested that the expression of miR-200 c in TPC-1 mimics group was significantly higher than that in NC group(P<0.001)and the expression level of miR-200 c in inhibitor group was significantly lower than that in NC group(P<0.001).Then western blot was performed to detect the expression of YWHAG,and the results showed that when miR-200 c was up-regulated,the expression of YWHAG was significantly decreased,and the expression of YWHAG was increased when the expression of miR-200 c was inhibited.4.TPC-1 cell line was treated with different concentrations of KI: 0μM,25μM,50μM and75μM,the results of western blot detection of YAWAG suggested that the expression of YAHAG in TPC-1 cells in the 50μM and 75μM KI treatment groups was downregulated compared with the 0um treatment group,while the expression of YWHAG in the 25μM treatment group was not significantly different from that in the control group.5.CCK-8 was used to detect the proliferation of cells when treated with different concentrations of KI solution after 12,24,36,48 hours :the proliferation rate of TPC-1 cells in 25μM,50μM and 75μM groups was higher than that in control group 0μM(P<0.05).Compared with mimics NC group,the overexpression of miR-200 c can significantly enhance the proliferation of TPC-1cells,while inhibition of miR-200 c expression inhibited the proliferation of TPC-1 cells.6.Scratch assay experiments suggested that TPC-1 cellswere cultured in different concentrations of KI solution after 48 hours,the cell migration was significantly enhanced in 50μM group and75μM group(P<0.05),and when the expression of miR-200 c was upregualted,the migration ability of TPC-1 was significantly increased compared with that of the control group.When the exression of miR-200 c was downregulated,the migration ability of TPC-1 was supressed.Conclusion:1.High iodine significantly increased miR-200 c expression in TPC-1 cell,but had no significant effect on miR-200 c expression in Nthy-ori 3-1 cells.2.High iodine stimulation and the overexpression of miR-200 c both promoted the process of TPC-1 cell proliferation and migration.3.The expression of miR-200 c decreased in papillary thyroid carcinoma cells,its overexpression promoted the process of TPC-1 cell proliferation and migration by inhibiting the expression of YWHAG.The miR-200c-YWHAG pathway in a high iodine environment was involved in the proliferation and migration of TPC-1cells.Our study further demonstrated the effect of miR-200 c in the biological process of TPC-1 cells under high iodine nutrition,and its clinical application as a potential molecular diagnostic and therapeutic target for human thyroid cancer needs further investigation. |
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