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目的:通过姜黄素对肠道肿瘤细胞miR-200a影响,明确其抑制肿瘤细胞EMT机理,揭示其抗肠道肿瘤侵袭转移机制。方法:以人结肠腺癌细胞HCT116为模型,采用PCR技术、基因重组技术、侵袭实验等一系列实验方法研究姜黄素对肿瘤细胞以下方面的影响:miR-200a表达水平,β-连环蛋白、波形蛋白、ZEB1、E-钙粘蛋白mRNA,细胞生长转化、侵袭转移。结果:与空白对照组比较,终浓度为3.68mg/L、7.36mg/L和14.73mg/L的姜黄素和3.00mg/L的顺铂可以显著抑制HCT116细胞软琼脂集落形成、HCT116细胞侵袭、HCT116细胞β-连环蛋白mRNA和波形蛋白mRNA表达、HCT116细胞ZEB1蛋白翻译,可以显著促进HCT116细胞microRNA-200a表达、促进E-钙粘蛋白蛋白翻译,姜黄素效应均表现出浓度依赖性。结论:姜黄素可以抑制肠道肿瘤细胞上皮间质转化的表型,即抑制HCT116软琼脂集落形成和细胞侵袭。其机制在于提高HCT116细胞microRNA-200a水平,抑制细胞β-连环蛋白mRNA、波形蛋白mRNA转录,抑制细胞ZEB1蛋白翻译、促进E-钙粘蛋白蛋白翻译。
Objective: To investigate the effect of curcumin on the expression of miR-200a in intestinal cancer cells and to clarify its mechanism of inhibiting the EMT of tumor cells and to reveal the mechanism of anti-invasion and metastasis of intestinal tumor. Methods: Human colon adenocarcinoma cell line HCT116 was used as a model to study the effects of curcumin on tumor cells using PCR, gene recombination and invasion assays. The expression of miR-200a, β-catenin, Protein, ZEB1, E-cadherin mRNA, cell growth transformation, invasion and metastasis. Results: Compared with the blank control group, curcumin at concentrations of 3.68 mg / L, 7.36 mg / L and 14.73 mg / L and cisplatin at 3.00 mg / L significantly inhibited the colony formation of soft agar and the invasion of HCT116 cells in HCT116 cells, HCT116 cells β-catenin mRNA and vimentin mRNA expression, HCT116 cells ZEB1 protein translation, can significantly promote HCT116 cells microRNA-200a expression, promote E-cadherin protein translation, curcumin effect showed a concentration-dependent. CONCLUSION: Curcumin can inhibit the phenotype of epithelial-mesenchymal transition of intestinal tumor cells, that is, inhibit the colony formation and cell invasion of HCT116 soft agar. The mechanism is to improve the level of microRNA-200a in HCT116 cells, inhibit the transcription of β-catenin mRNA and vimentin mRNA, inhibit the translation of ZEB1 protein and promote the translation of E-cadherin protein.