检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:廖晓敏[1] 孙双凌[2] 汤为学[3] 赖洁娟[1] 蒲淑萍[1]
机构地区:[1]重庆医科大学细胞生物学及遗传学教研室,重庆400016 [2]重庆医药高等专科学校,重庆400030 [3]重庆医科大学病理生理学教研室,重庆400016
出 处:《西南师范大学学报(自然科学版)》2009年第1期141-145,共5页Journal of Southwest China Normal University(Natural Science Edition)
摘 要:为研究缺氧诱导因子-1α(HIF-1α)在人乳腺癌细胞中的表达及其与乳腺癌细胞侵袭转移能力的相关性,采用在培养基中加入CoC12模拟化学缺氧培养细胞,RT-PCR和Western-blot、免疫细胞化学检测HIF-1α在人乳腺癌细胞MCF-7和MDA-MB-231中mRNA水平和蛋白质水平在缺氧前后的表达差异,及Millicell小室人工重组基底膜侵袭迁移实验检测缺氧前后两株细胞侵袭迁移能力的改变.结果发现:缺氧后,两株细胞的HIF-1αmRNA水平和蛋白质水平均较缺氧前增高(p<0.01),MDA-MB-231和MCF-7之间有显著差异(p<0.01);MDA-MB-231的侵袭转移能力明显增加(p<0.01),MCF-7的侵袭转移能力略有增加(p<0.05).表明缺氧上调HIF-1α转录及蛋白表达,进而促进乳腺癌细胞的侵袭转移能力.To investigate the expression of HIF-1α(Hypoxia-inducible factor -1α) under hypoxic induced by CoCl2, and the correlation between the expression of HIF -1α and invasion and metasis potential of human breast cancer cell line, the mRNA expression level of HIF -1α was detected by RT - PCR, and the protein expression level of HIF -1α was measured by Western blotting and Immunocytochemistry, the effects of HIF -1α on the invasion and motility abilities of human breast cancer line MCF - 7 and MDA : MB- 231 in vitro were explored by millicell chamber. All the tests of hypoxia were induced by CoCl2. It was found that the endounous expression of HIF -1α mRNA and the protein expression level of HIF -1α under hypoxia than normoxia in MCF- 7 and MDA -MB- 231(p〈0.01), there were endounous difference between MCF - 7 and MDA - MB - 231 (p〈0.01) . the invasive and metastatic potential in MCF - 7 and MDA - MB - 231 were raised significantly(p〈0.05), but MDA - MB - 231 cell was more significant than that of MCF- 7 cell(p〈0. 01). It is concluded that Hypoxia promotes breast cancer cells MCF - 7 and MDA - MB - 231 invasion and metastasis by inducing the up-regulation HIF -1α expression.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.38