CAJ | 학술논문

邻苯二甲酸二丁酯(DBP)在体外对肺巨细胞癌细胞(PG)和人早幼粒白血病细胞(HL-60)的增殖有明显的抑制作用；经DBP处理过的PG细胞，DNA断裂，在琼脂糖凝胶电泳上呈现出特异的断裂带；流式细胞术分析表明，DBP能提高PG细胞的凋亡率，并且随作用时间的延长而增大；斑点杂交的结果显示，被DBP处理过的HL-60细胞中某些原癌基因、抑癌基因和肿瘤抑制基因的mRNA表达水平都有所下降，这提示DBP对HL-60细胞增殖抑制作用的机制之一可能是通过抑制这些癌基因和突变的抑癌基因的表达来实现的.
린분이갑산이정지(DBP)재체외대폐거세포암세포(PG)화인조유립백혈병세포(HL-60)적증식유명현적억제작용；경DBP처리과적PG세포，DNA단렬，재경지당응효전영상정현출특이적단렬대；류식세포술분석표명，DBP능제고PG세포적조망솔，병차수작용시간적연장이증대；반점잡교적결과현시，피DBP처리과적HL-60세포중모사원암기인、억암기인화종류억제기인적mRNA표체수평도유소하강，저제시DBP대HL-60세포증식억제작용적궤제지일가능시통과억제저사암기인화돌변적억암기인적표체래실현적.
Dibutyl phthalate (DBP) showed significant inhibitory effect on the proliferation of lung cancer cells (PG) and leukemic cells (HL-60) in vitro. With the exposure of PG cells to DBP, DNA degraded in certain way produced specific fragments on agarose gel electrophoresis. Flow cytometric analysis indicated that DBP enhanced the apoptotic rate of PG cells, which depended on the duration of interaction. The results of dot blotting demonstrated that the mRNA expression level of c-H-ras， c-myc，Rb，p53 and bcl-2 in HL-60 cells treated by DBP decreased, which implicated that the suppression of DBP on the expression of the these oncogenes and mutant tumor suppressor genes may be one of the mechanisms by which DBP inhibiting the HL-60 cell proliferation.