發(fā)布時間：2018-05-24 03:10

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

【摘要】：目的建立耐紫杉醇食管癌(EC)細胞系EC9706/PTX,觀察姜黃素對EC9706/PTX細胞上皮間質(zhì)轉(zhuǎn)化(EMT)的抑制作用并探討其機制,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細胞EC9706/PTX,四甲基偶氮唑藍(MTT)法測定細胞耐藥指數(shù)及交叉耐藥性,檢測不同濃度姜黃素對EC9706/PTX細胞增殖的抑制。使用細胞骨架染色、劃痕實驗、Transwell侵襲實驗檢測姜黃素對EC9706/PTX細胞形態(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)檢測姜黃素對EC9706/PTX細胞中EMT相關(guān)分子標志物E-鈣黏蛋白、N-鈣黏蛋白、波形蛋白、纖維連接蛋白在mRNA和蛋白水平的表達影響。Western blot檢測姜黃素對EC9706/PTX細胞中轉(zhuǎn)錄因子NF-κB p65及Snail在蛋白水平的表達影響。結(jié)果 EC9706/PTX對紫杉醇的耐藥指數(shù)為28.4,對順鉑、阿霉素產(chǎn)生交叉耐藥性,姜黃素能夠抑制EC9706/PTX細胞的增殖。在20μmol/L濃度的姜黃素作用下,EC9706/PTX細胞的遷移和侵襲能力明顯降低。熒光定量PCR及Western blot檢測顯示,細胞耐藥后E-鈣黏蛋白的表達明顯下調(diào),而N-鈣黏蛋白表達則明顯上調(diào),姜黃素逆轉(zhuǎn)了這一現(xiàn)象。Western blot檢測提示,EC細胞發(fā)生耐藥及EMT后,NF-κB p65及Snail蛋白的表達增強,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細胞的增殖并且能夠逆轉(zhuǎn)紫杉醇耐藥EC細胞的EMT現(xiàn)象,其機制可能是通過抑制NF-κB-Snail信號通路實現(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)與前沿項目(112300410044)
【分類號】：R735.1

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