本文選題：乳腺癌 + TR1��； 參考：《蘭州大學(xué)》2017年碩士論文

【摘要】：目的:甲狀腺素受體β1與人多種腫瘤的發(fā)生發(fā)展有關(guān),但其在乳腺癌的作用及作用機(jī)理還不是很清楚。我們本次研究利用脂質(zhì)體轉(zhuǎn)染法使甲狀腺素受體β1高表達(dá)于乳腺癌細(xì)胞株,檢測(cè)該受體對(duì)乳腺癌細(xì)胞增殖能力的影響,并探索發(fā)揮該作用的機(jī)制。方法:挑選出兩株乳腺癌細(xì)胞MCF-7和MDA-MB-231,用脂質(zhì)體將THRB基因轉(zhuǎn)染于乳腺癌細(xì)胞中,使乳腺癌細(xì)胞高表達(dá)甲狀腺素受體β1,并利用免疫印記(western blotting/WB)的方法測(cè)定轉(zhuǎn)染效率,確保轉(zhuǎn)染有效。并在蛋白水平上檢測(cè)PI3K-AKT-mTOR通路蛋白在三組中的改變。結(jié)果:免疫印記實(shí)驗(yàn)證實(shí)轉(zhuǎn)染有效,MTT檢測(cè)結(jié)果顯示高表達(dá)TRβ1的細(xì)胞組增殖能力較空白對(duì)照組和轉(zhuǎn)染空質(zhì)粒組降低,Western Blotting檢測(cè)蛋白水平:轉(zhuǎn)染TRβ1組較其余兩組p-AKT、p-mTOR表達(dá)低,總AKT、mTOR在三組之間無(wú)差異。加入配體T3后,隨T3濃度的增高,p-AKT、p-mTOR的表達(dá)降低,表現(xiàn)出T3依賴性,總AKT、mTOR無(wú)差異。結(jié)論:TRβ1抑制乳腺癌細(xì)胞增殖,抑制PI3K/AKT/mTOR下游通路的AKT/mTOR的活化。在其配體T3存在的情況下,TRβ1對(duì)乳腺癌細(xì)胞的抑制作用增強(qiáng),對(duì)p-AKT/p-mTOR通路抑制也增強(qiáng)。
[Abstract]:Objective: thyroxine receptor 尾 1 is associated with the occurrence and development of many kinds of human tumors, but its role and mechanism in breast cancer is not clear. In this study, thyroxine receptor 尾 1 was overexpressed in breast cancer cell line by liposome transfection, and the effect of thyroxine receptor on proliferation of breast cancer cell line was detected, and the mechanism of this effect was explored. Methods: two breast cancer cell lines, MCF-7 and MDA-MB-231, were selected. The THRB gene was transfected into breast cancer cells by liposome. The expression of thyroxine receptor 尾 1 was detected by Western blotting. The transfection efficiency was determined by Western blotting. The changes of PI3K-AKT-mTOR pathway proteins in the three groups were detected at the protein level. Results: the results of immunoimprinted assay showed that the proliferative ability of the cells with high expression of tr 尾 1 was lower than that of the blank control group and the empty plasmid group. The expression of p-AKTN p-mTOR in the transfected tr 尾 1 group was lower than that in the other two groups. There was no difference in total AKT mTOR among the three groups. When the ligand T3 was added, the expression of p-AKTO p-mTOR decreased with the increase of T3 concentration, and the expression of p-mTOR was T3 dependent. There was no difference in total AKTT mTOR. Conclusion: tr 尾 1 inhibits the proliferation of breast cancer cells and inhibits the activation of AKT/mTOR in the downstream pathway of PI3K/AKT/mTOR. The inhibitory effect of tr 尾 1 on breast cancer cells was enhanced in the presence of its ligand T3, and the inhibition of p-AKT/p-mTOR pathway was also enhanced.
【學(xué)位授予單位】：蘭州大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R737.9

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本文編號(hào)：1979184