| Objective To observe whether 17?-estradiol affects the proliferation and migration of thyroid papillary carcinoma cell TPC-1 through MAPK signaling pathway.Methods To regulate the cultivation of human thyroid papillary carcinoma cell TPC-1,when the cell condition is better,replace the medium without endogenous estrogen,and add 17?-estradiol medium containing different concentrations of 10-4M?10-9M incubate for 24 hours,48 hours,72 hours,96 hours,and use the CCK-8 experiment to detect the optical density?OD value?of each group of cells to observe the proliferation of cells.According to the OD value,determine the best effective concentration of estrogen and the treatment time;human papillary thyroid carcinoma cells pretreated with endogenous estrogen medium were divided into 4 groups: blank control group,estrogen group,inhibitor group,estrogen plus inhibitor group.The CCK-8 experiment was used to detect the optical density?OD?of each group of cells to observe cell proliferation;the scratch experiment was used to detect the migration ability of each group of cells;the Western blot was used to detect the activity of the downstream protein Erk1/ 2 of the MAPK signaling pathway.Results 1 After pretreatment,human thyroid papillary carcinoma cells were replaced with different concentrations of 17?-estradiol medium.The CCK-8 experiment was used to detect the OD value of each group of cells to determine that 10-7M 17?-estradiol was being treated.The cell value-added effect was the best at 96 h,and this concentration was selected for subsequent experiments.2 The CCK-8 experiment showed that the OD value of the estrogen group?1.015±0.026?was significantly higher than that of the blank control group?0.9170 ± 0.028?at 96 h and estrogen plus inhibitor group?0.942±0.057?,the difference was statistically significant?P<0.05?,indicating that 17?-estradiol can promote the proliferation of thyroid papillary carcinoma cells,and this effect can be inhibited by MAPK signaling pathway Blocked.3 The results of the scratch test showed that the cell migration rate?0.871±0.015?of the estrogen group was significantly greater than that of the blank control group?0.640±0.041?and the estrogen plus inhibitor group?0.569±0.021?at 24 h.The difference was statistically significant?P<0.05?,indicating that17?-estradiol can promote the migration of papillary thyroid cancer cells,and this effect can be blocked by MAPK signaling pathway inhibitors.4 Western blot results showedthat compared with the blank control group?0.490±0.026?,the expression of p-Erk1/2protein?0.893±0.025?in the estrogen group was significantly increased at 96 h,and the difference was statistically significant?P<0.05?,indicating that 17?-estradiol can activate the Erk1/2 protein downstream of the MAPK signaling pathway.Conclusion Estrogen enhances the proliferation and migration ability of human thyroid papillary carcinoma cell TPC-1 by activating MAPK signaling pathway.The use of MAPK inhibitors can inhibit the effect of estrogen.Therefore,targeting estrogen / MAPK may provide a new way for the treatment of thyroid papillary carcinoma.Figure 4;Table 3;Reference 124... |
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