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目的:探讨胃癌细胞奥沙利铂(oxaliplatin,L-OHP)耐药与上皮-间质转化(EMT)的关系。方法:采用逐步递增L-OHP浓度持续体外诱导人胃癌SGC-7901细胞,建立L-OHP耐药细胞系SGC-7901/L-OHP;通过形态学、群体倍增时间、药物敏感性检测确定SGC-7901/L-OHP成功建立;比较SGC-7901/L-OHP细胞与亲代细胞EMT相关标记物N-cadherin和E-cadherin表达差异。结果:经6个月诱导,L-OHP耐药细胞系SGC-7901/L-OHP成功建立,表现为该细胞的形态由上皮表型转变为间质样细胞表型;群体倍增时间较亲代细胞明显延长(P<0.05);L-OHP的IC50为亲代细胞的9.7倍。与亲代细胞SGC-790比较,SGC-7901/L-OHP细胞中N-cadherin m RNA和蛋白表达明显上调,E-cadherin m RNA和蛋白表达明显下调(均P<0.05)。结论:EMT可能是人胃癌细胞对L-OHP产生耐药的重要机制。
Objective: To investigate the relationship between drug resistance and epithelial-mesenchymal transition (EMT) of gastric cancer cell oxaliplatin (L-OHP). Methods: SGC-7901 cells were induced by gradually increasing concentration of L-OHP in vitro, and the cell line SGC-7901 / L-OHP was established. The morphological, doubling time and drug sensitivity of SGC- 7901 / L-OHP was successfully established. The differences of expression of EMT-related markers N-cadherin and E-cadherin between SGC-7901 / L-OHP cells and their parental cells were compared. Results: After 6 months of induction, L-OHP-resistant cell line SGC-7901 / L-OHP was successfully established, which showed that the morphology of the cells changed from epithelial phenotype to mesenchyme-like phenotype; population doubling time was longer than that of parental cells (P <0.05). The IC50 of L-OHP was 9.7 times of that of parental cells. The expression of N-cadherin mRNA and protein in SGC-7901 / L-OHP cells was significantly up-regulated compared with parental SGC-790 cells, and the expression of E-cadherin m RNA and protein were significantly down-regulated (all P <0.05). Conclusion: EMT may be an important mechanism of human gastric cancer cell resistance to L-OHP.