耐药人乳腺癌细胞株Bcap37/MDR1及其亲本细胞株Bcap37 ^(18)F-FDG细胞结合实验的比较研究

Comparative studies of the ^(18)F-FDG cell binding the drug-resistant breast cancer cell Bcap37/MDR1 and breast cancer cell Bcap37

对耐药人乳腺癌细胞株Bcap37/MDR1与其亲本细胞株Bcap3718F-FDG结合率进行比较,为进一步研究化疗药物对两细胞株抑制的实验研究奠定基础。方法:在不同条件下分别测定18F-FDG与Bcap37/MDR1和Bcap37的结合率。①细胞数为1.25×105~1×107个/瓶;②反应时间为20~120min;③18F-FDG放射性活度为1.85~29.6 KBq;④葡萄糖的浓度为0~5.5 mmol/L。用γ测量仪测量细胞的CPM计数(B)及上清液CPM计数(F),计算18F-FDG的细胞结合率(%)=(B/(B+F))×100%,并行两者差异的比较。结果:当其它条件不变,分别改变细胞数量、反应时间、18F-FDG放射性活度时,Bcap37结合率均高于Bcap37/MDR1,两组差异均有统计学意义(P<0.05)。当其它条件不变,葡萄糖的浓度为0 mmol/L和1.39 mmol/L时,两组细胞间结合率差异均有统计学意义(P<0.05);葡萄糖的浓度为2.78 mmol/L和5.5 mmol/L时,两组细胞间结合率差异均无统计学意义(P>0.05)。结论:在各种实验条件下,Bcap37/MDR1的18F-FDG细胞结合率均低于Bcap37,表明耐药肿瘤细胞的增殖及代谢均低于其亲本肿瘤细胞。

Objective： To compare the lSF-FDG cell binding in the drug-resistan breast cancer cell Bcap37/MDR1 and breast cancer cell Beap37, to lay the foundation for a further study of the inhibitory effect of chemotherapy in breast cancer cell Bcap37/MDR1 and breast cancer cell Bcap37. Methods： Several different binding conditions were tested. （1）The cell number was 1.25x10^5x10^7/bottle. （2）The reaction time was 20-120 rain. （3）The radioactivity of ISF-FDG was 1.85-29.6 KBq. @The glucose concentration was 0-5.5 mmol/L. The count of CPM （B） in cells and CPM （F） in supernatant were measured by the equipment. The binding efficiency of Bcap37 and Bcap37/MDR1 cell with lSF-FDG were calculated and compared. Result： When other conditions were invariable, and separately changed cell number, the reaction time and the lSF-FDG ra- dioactivity, the binding efficiency of Bcap37 was higher than the Bcap37/MDR1. The difference was significant （P〈0.05）. The difference of binding efficiency between Bcap37 and Bcap37/MDR1 cell at the 0 and 1.39 mmol/L groups was significant （P〈 0.05）; The difference of binding efficiency between Bcap37 and Bcap37/MDR1 cell at 2.78 mmol/L and 5.5 mmol/L groups was not statistically significant（P〉0.05）. Conclusions： The lSF-FDG cell binding of breast cancer Bcap37/MDR1 was lower than the Bcap37. It showed that the proliferation and metabolism of drug resistance of tumor cells were lower than the parental tumor cells.