Pancreatic carcinoma is a group of cancer that seriously threatens human life, to which chemotherapy is one of the most important treatments. Although in recent years, new chemotherapy drugs and regimens have been introduced, drug resistance has been a chief cause for the failure of chemotherapy. The chemotherapy sensitivity test for carcinoma used in the past was based on monolayer cultured cells in a two-dimensional model, while the pancreatic cancer cells in the human body survive in a three-dimensional growing model. Monolayer cultured cells model neglects the different characteristics between a whole tumor and its individual tumor cell as well as the interactions between tumor cells and the impacts of the microenvironment. More and more researches in recent years show that the interaction between tumor cells and the microenvironment is the basis for tumor growth and survival, which may be involved in the regulation of drug reactions and the incidence of cancer drug resistance. Multidrug-resistance (MDR) is the major reason for failure of cancer therapy. P-glycoprotein (P-gp), which is encoded by MDR1gene, confers resistance to certain anticancer agents. P-gp/MDR1is found in various human tissues in addition to being expressed in tumours cells.Ovarian cancer multicellular spheroids cultures induced cell resisitance to Taxol. High expression of P-gp was induced in ovarian multicellular spheroids. The expression of P-gp was argumentative. In this study, pancreatic cell lines Aspc-1,Bxpc-3and Sw-1990were cultivated in both two-dimensional and three-dimensional. Real time PCR was employed to detect Mdrl while expression of P-gp was determined using Western blot analysis. Drug sensitivity was tested either. Pancreatic cancer Aspc-1, Bxpc-3, Sw-1990multicellular spheroids cultures induced cell resistance to Gemcitabine. High expression of P-gp was induced in Aspc-1and Bxpc-3multicellular spheroids. |