地砷病区乳腺癌致病机制研究  

Study on Pathogenic Mechanism of Breast Cancer in Arsenic Ward

作　　者：张明明[1] 李婷[2] 郑春雨[2] 董雪[2] 

机构地区：[1]吉林省人民医院,吉林长春130021 [2]长春中医药大学

出　　处：《中国实验诊断学》2017年第6期1064-1066,共3页Chinese Journal of Laboratory Diagnosis

基　　金：吉林省教育厅项目(20163)

摘　　要：目的研究亚砷酸钠(NaAsO_2)对小鼠乳腺上皮细胞(NMuMG)增殖的抑制作用机制,为地砷病区乳腺癌致病机制提供理论依据。方法以不同浓度的NaAsO_2(0,5,10,20,30μM)处理的NMuMG,观察其形态的变化;经Cell Counting Kit-8(CCK-8)测定不同浓度NaAsO_2对NMuMG增殖情况;用实时定量RT-PCR分析增殖基因c-myc mRNAs的表达水平。结果在一定浓度范围内,随亚砷酸钠浓度升高,其细胞间隙变宽、形状不规则,甚至凋亡。在一定浓度范围内,随着NaAsO_2浓度增高其增殖明显受到抑制,呈明确的剂量-效应关系;20μM NaAsO_2使c-myc mRNA表达水平明显降到11%。结论亚砷酸钠抑制NMuMG的增殖是通过降低增殖基因c-myc的表达来实现的,这是地砷病区乳腺癌疾病高发的原因之一。Objective The studies were carried out to explore the effect of sodium arsenite on the proliferation of mouse mammary epithelial cells （NMuMG） and its molecular mechanisms. Methods The changes of NMuMG were observed by Cell Counting Kit 8 （CCK-8） at different concentrations of NaAsO2 （0,5,10,20,30 μM）. The proliferation of NMuMG was determined by real-time quantitative RT The expression of proliferating gene c-myc mRNAs was ana lyzed by PCR. Results In a certain concentration range, with the concentration of sodium arsenate increased, the cell gap widened,irregular shape,and even apoptosis. In a certain concentration range, the proliferation was significantly in- hibited with the increase of NaAsO2 concentration, showing a clear dose effect relationship;20 μM NaAsO2 significantly reduced the expression of c-myc mRNA to 11%. Conclusion and Discussion： Sodium arsenite may further inhibit the proliferation of NMuMG by downregulating the expression of c myc gene,which may be one of the mechanisms of en demic arsenic poisoning leading to breast cancer.

关 键 词：亚砷酸钠 增殖 C-MYC 

分 类 号：R737.9[医药卫生—肿瘤]