Study On The Regulatory Effect Of Non-coding RNA-143 (MIR143) On Papillary Thyroid Carcinoma

Aim: The purpose of this study was to determine the mechanism of mi R-143 targeting TSHR methylation to regulate K1 proliferation in PTC cells.Methods: Real-time quantitative PCR was used to identify the mRNA expression of mi R-143 and TSHR in PTC tissues and cells.Western blot was used to identify the protein expression of TSHR.Mi R-143-mimic and its control were transfected in K1 cells to identify the expression of TSHR and cells Proliferation,cell proliferation was detected using the CCK8 kit method,and sh TSHR and its controls were transfected in K1 cells to identify cell proliferation;mi R-143-mimic and its controls were transfected in K1 cells to use methylation specificity PCR was used to detect changes in methylation levels of TSHR,and detect changes in protein expression of DNMT3 A.Finally,sh TSHR and its controls were transfected in K1 cells and treated with Perk pathway activators to identify protein expressions of TSHR,phosphorylated Perk,Perk,and MMP9.Changes in conditions and cell proliferation.Results: Compared with paracancerous tissues and Nthy-ori 3-1 cells,mi R-143 expression was reduced and TSHR expression was increased in PTC tissues and K1 cells.Compared with the transfected mi R-143-con group,mi R-143-mimic overexpression inhibited K1 cell proliferation and decreased TSHR expression;compared with transfected sh RNA-con group,inhibited TSHR expression inhibited K1 cell proliferation.Compared with Nthy-ori 3-1 group and transfected mi R-143-con group,the methylation level of TSHR in mi R-143-mimic group was enhanced,and protein expression of DNMT3 A increased.Compared with the K1 + sh RNA-con group,the K1 + sh RNA-TSHR group had reduced TSHR,phosphorylated p ERK1/2,MMP9 protein expression,and inhibited cell proliferation.The activator treated the K1 + sh RNA-TSHR group with TSHR and phosphorylated p ERK1/2,MMP9 protein expression increased,and cell proliferation trend recovered;there's no difference of total ERK1/2 protein expression in three groups.Conclusion: mi R-143 may inhibit ERK signaling pathway by regulating TSHR methylation level,thereby suppressing PTC cell proliferation.