本文選題：紫杉醇 + 食管腫瘤��； 參考：《重慶醫(yī)學(xué)》2017年34期

【摘要】：目的建立耐紫杉醇食管癌(EC)細(xì)胞系EC9706/PTX,觀察姜黃素對(duì)EC9706/PTX細(xì)胞上皮間質(zhì)轉(zhuǎn)化(EMT)的抑制作用并探討其機(jī)制,為耐藥EC的治療提供理論依據(jù)。方法用中等濃度間歇作用法建立耐紫杉醇EC細(xì)胞EC9706/PTX,四甲基偶氮唑藍(lán)(MTT)法測(cè)定細(xì)胞耐藥指數(shù)及交叉耐藥性,檢測(cè)不同濃度姜黃素對(duì)EC9706/PTX細(xì)胞增殖的抑制。使用細(xì)胞骨架染色、劃痕實(shí)驗(yàn)、Transwell侵襲實(shí)驗(yàn)檢測(cè)姜黃素對(duì)EC9706/PTX細(xì)胞形態(tài)變化、遷移和侵襲能力的影響。熒光定量PCR及蛋白免疫印跡(Western blot)檢測(cè)姜黃素對(duì)EC9706/PTX細(xì)胞中EMT相關(guān)分子標(biāo)志物E-鈣黏蛋白、N-鈣黏蛋白、波形蛋白、纖維連接蛋白在mRNA和蛋白水平的表達(dá)影響。Western blot檢測(cè)姜黃素對(duì)EC9706/PTX細(xì)胞中轉(zhuǎn)錄因子NF-κB p65及Snail在蛋白水平的表達(dá)影響。結(jié)果 EC9706/PTX對(duì)紫杉醇的耐藥指數(shù)為28.4,對(duì)順鉑、阿霉素產(chǎn)生交叉耐藥性,姜黃素能夠抑制EC9706/PTX細(xì)胞的增殖。在20μmol/L濃度的姜黃素作用下,EC9706/PTX細(xì)胞的遷移和侵襲能力明顯降低。熒光定量PCR及Western blot檢測(cè)顯示,細(xì)胞耐藥后E-鈣黏蛋白的表達(dá)明顯下調(diào),而N-鈣黏蛋白表達(dá)則明顯上調(diào),姜黃素逆轉(zhuǎn)了這一現(xiàn)象。Western blot檢測(cè)提示,EC細(xì)胞發(fā)生耐藥及EMT后,NF-κB p65及Snail蛋白的表達(dá)增強(qiáng),姜黃素阻斷了這一作用。結(jié)論姜黃素能夠抑制紫杉醇耐藥EC細(xì)胞的增殖并且能夠逆轉(zhuǎn)紫杉醇耐藥EC細(xì)胞的EMT現(xiàn)象,其機(jī)制可能是通過(guò)抑制NF-κB-Snail信號(hào)通路實(shí)現(xiàn)的。
[Abstract]:Objective to establish paclitaxel-resistant esophageal carcinoma cell line EC9706 / PTX. to observe the inhibitory effect of curcumin on epithelial mesenchymal transformation of EC9706/PTX cells and its mechanism, and to provide a theoretical basis for the treatment of drug-resistant EC. Methods Taxol-resistant EC cells EC9706 / PTX and tetramethylazolam MTT were used to determine the drug resistance index and cross resistance. The inhibition of curcumin at different concentrations on the proliferation of EC9706/PTX cells was detected. The effects of curcumin on the morphological changes, migration and invasion of EC9706/PTX cells were detected by cytoskeleton staining and transwell invasion assay. Fluorescence quantitative PCR and Western blot were used to detect the effect of curcumin on EMT related molecular marker E-cadherin and vimentin in EC9706/PTX cells. The expression of fibronectin at mRNA and protein levels. Western blot was used to detect the expression of transcription factor NF- 魏 B p65 and Snail in EC9706/PTX cells. Results the resistance index of EC9706/PTX to paclitaxel was 28. 4, cross resistance to cisplatin and adriamycin. Curcumin could inhibit the proliferation of EC9706/PTX cells. The migration and invasion ability of EC9706 / PTX cells was significantly decreased at 20 渭 mol/L concentration of curcumin. Fluorescence quantitative PCR and Western blot analysis showed that the expression of E-cadherin was down-regulated, while the expression of N- cadherin was up-regulated. Curcumin reversed this phenomenon. Western blot assay showed that the cells developed drug resistance and the expression of NF- 魏 B p65 and Snail protein increased after EMT, which was blocked by curcumin. Conclusion curcumin can inhibit the proliferation of paclitaxel-resistant EC cells and reverse the EMT phenomenon of paclitaxel-resistant EC cells. The mechanism may be through the inhibition of NF- 魏 B-Snail signaling pathway.
【作者單位】： 鄭州大學(xué)附屬腫瘤醫(yī)院/河南省腫瘤醫(yī)院消化內(nèi)一科;
【基金】：河南省科技廳基礎(chǔ)與前沿項(xiàng)目(112300410044)
【分類號(hào)】：R735.1

【相似文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前1條

1 衛(wèi)佳麗;姜黃素聯(lián)合紫杉醇對(duì)人肺腺癌A549細(xì)胞株生物學(xué)效應(yīng)的影響[D];西南醫(yī)科大學(xué);2017年

，

本文編號(hào)：1927453