雌激素受体α36介导雌激素促进甲状腺乳头状癌细胞增殖的分子机制

发布时间：2018-06-17 07:15

本文选题：雌激素受体α + 雌激素　；参考：《第三军医大学学报》2017年24期

【摘要】：目的研究雌激素受体α36(estrogen receptor alpha-36,ERα36)介导雌激素促进甲状腺乳头状癌(papillary thyroid carcinoma,PTC)细胞增殖的分子机制及相关信号通路。方法采用免疫组化(S-P)检测ERα36在34例人PTC组织标本及其21例配对癌旁组织标本中的表达;梯度浓度E2(0、10~(-7)、10~(-8)、10~(-9)mol/L)处理PTC细胞株K-1和BCPAP后,Western blot检测两种细胞株中ERα36的表达;10-8mol/L E2处理后,Western blot检测两种细胞株ERK1/2和AKT磷酸化水平的变化,以及ERα36-si RNA对其的抑制作用;梯度浓度的E2处理BCPAP细胞后,MTT法检测细胞增殖和ERα36-si RNA对增殖的抑制作用。结果在人PTC组织中ERα36的阳性表达率为82.4%,明显高于癌旁组织(P0.05)。PTC细胞株K-1和BCPAP均表达ERα36;10-8mol/L E2处理细胞后,ERα36的表达增高,且呈时间依赖性。E2能促进BCPAP和K-1细胞ERK1/2和AKT蛋白磷酸化水平增高,且处理15 min时BCPAP细胞最明显,10 min时K-1细胞最明显,而ERα36-si RNA能抑制E2的诱导效果;E2促进BAPAP细胞增殖,ERα36-si RNA则抑制E2的诱导效果。结论 ERα36通过ERK/AKT途径介导雌激素促进PTC细胞增殖。
[Abstract]:Objective to investigate the molecular mechanism of estrogen receptor 伪 36(estrogen receptor alpha-36 (ER 伪 36) mediated by estrogen in promoting the proliferation of papillary thyroid (PTC) cells and its related signaling pathways. Methods Immunohistochemical staining was used to detect the expression of ER 伪 36 in 34 human PTC tissues and 21 matched paracancerous tissues. The expression of ER 伪 36 in PTC cell line K-1 and BCPAP was detected by Western blot after the treatment with gradient concentration of E2 / 10 ~ (-10) mol / L ~ (-8) ~ 10 ~ (-8) mol 路L ~ (-1) and 10 ~ (-8) mol / L E ~ (2), and the phosphorylation level of ERK1 / 2 and AKT was detected by Western blot, and the inhibitory effect of ER 伪 36-si RNA on the expression of ER 伪 _ (36) was also detected. The proliferation of BCPAP cells and the inhibitory effect of ER 伪 36-si on the proliferation of BCPAP cells were detected by MTT assay. Results the positive expression rate of ER 伪 36 in human PTC tissue was 82.4%, which was significantly higher than that in P0.05 PTC cell line K-1 and BCPAP. The expression of ER 伪 36 was increased after treated with 10 ~ (-8) mol / L E _ 2. In a time-dependent manner, E2 could increase the phosphorylation of ERK1 / 2 and AKT protein in BCPAP and K-1 cells, and the K-1 cells were the most obvious at 10 min after 15 min treatment. On the other hand, ER 伪 36-si can inhibit the induction of E 2. The effect of E 2 on the proliferation of BAPAP cells was inhibited by ER 伪 36-si. Conclusion ER 伪 36 mediates the proliferation of PTC cells via ERK / AKT pathway.
【作者单位】：重庆医科大学分子医学与肿瘤研究中心;
【基金】：国家自然科学基金面上项目(81272937)~~
【分类号】：R736.1

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