肿瘤研究与临床
腫瘤研究與臨床
종류연구여림상
CANCER RESEARCH AND CLINIC
2012年
4期
217-219
,共3页
蒋富强%温居一%康静波%聂青
蔣富彊%溫居一%康靜波%聶青
장부강%온거일%강정파%섭청
乳腺肿瘤%缺氧%上皮%间质细胞%肿瘤浸润%细胞迁移
乳腺腫瘤%缺氧%上皮%間質細胞%腫瘤浸潤%細胞遷移
유선종류%결양%상피%간질세포%종류침윤%세포천이
Breast neoplasms%Anoxia%Epithelium%Stromalcells%Neoplasm invasiveness%Cel migration
目的 探讨缺氧对人类乳腺癌细胞MCF-7上皮-间质转化(EMT)标志分子E-钙黏着素( E-cadherin)、波型蛋白(Vimentin)及侵袭迁移能力的影响,揭示缺氧引起乳腺癌侵袭转移的机制,为临床治疗乳腺癌提供实验及理论依据.方法 采用Western blot检测低氧诱导因子-1α( HIF-1α)、E-cadherin、Vimentin的变化；四甲基偶氮唑蓝(MTT)法检测缺氧对人类乳腺癌细胞MCF-7黏附能力的影响；Transwell侵袭小室法检测缺氧对MCF-7细胞侵袭和迁移能力的影响.结果 随着缺氧时间的延长,人类乳腺癌细胞中E-cadherin表达明显降低(0.09±0.02)(t=30.98,P=0.0007),Vimentin表达明显升高( 0.69±0.04)(f=915,P=0.0000)；缺氧72 h组MCF-7细胞黏附(81.23±0.74) (t=82.05,P=0.000)、侵袭(120±6)(t=22.78,P=0.0009)和迁移能力明显增强(190±6)(t=23.49,P=0.000).结论 缺氧能下调E-cadherin、上调Vimentin而引起EMT的发生,促进MCF-7细胞黏附、侵袭和迁移.
目的 探討缺氧對人類乳腺癌細胞MCF-7上皮-間質轉化(EMT)標誌分子E-鈣黏著素( E-cadherin)、波型蛋白(Vimentin)及侵襲遷移能力的影響,揭示缺氧引起乳腺癌侵襲轉移的機製,為臨床治療乳腺癌提供實驗及理論依據.方法 採用Western blot檢測低氧誘導因子-1α( HIF-1α)、E-cadherin、Vimentin的變化；四甲基偶氮唑藍(MTT)法檢測缺氧對人類乳腺癌細胞MCF-7黏附能力的影響；Transwell侵襲小室法檢測缺氧對MCF-7細胞侵襲和遷移能力的影響.結果 隨著缺氧時間的延長,人類乳腺癌細胞中E-cadherin錶達明顯降低(0.09±0.02)(t=30.98,P=0.0007),Vimentin錶達明顯升高( 0.69±0.04)(f=915,P=0.0000)；缺氧72 h組MCF-7細胞黏附(81.23±0.74) (t=82.05,P=0.000)、侵襲(120±6)(t=22.78,P=0.0009)和遷移能力明顯增彊(190±6)(t=23.49,P=0.000).結論 缺氧能下調E-cadherin、上調Vimentin而引起EMT的髮生,促進MCF-7細胞黏附、侵襲和遷移.
목적 탐토결양대인류유선암세포MCF-7상피-간질전화(EMT)표지분자E-개점착소( E-cadherin)、파형단백(Vimentin)급침습천이능력적영향,게시결양인기유선암침습전이적궤제,위림상치료유선암제공실험급이론의거.방법 채용Western blot검측저양유도인자-1α( HIF-1α)、E-cadherin、Vimentin적변화；사갑기우담서람(MTT)법검측결양대인류유선암세포MCF-7점부능력적영향；Transwell침습소실법검측결양대MCF-7세포침습화천이능력적영향.결과 수착결양시간적연장,인류유선암세포중E-cadherin표체명현강저(0.09±0.02)(t=30.98,P=0.0007),Vimentin표체명현승고( 0.69±0.04)(f=915,P=0.0000)；결양72 h조MCF-7세포점부(81.23±0.74) (t=82.05,P=0.000)、침습(120±6)(t=22.78,P=0.0009)화천이능력명현증강(190±6)(t=23.49,P=0.000).결론 결양능하조E-cadherin、상조Vimentin이인기EMT적발생,촉진MCF-7세포점부、침습화천이.
Objective To study the effect of hypoxia on EMT molecule E-cadherin, Vimentin and invasion of human breast cancer MCF-7 cells, reveal the mechanism of breast cancer invasion and metastasis and provide experimental and theoretical basis. Methods Western blot was used to observe the change of HIF-1α, E-cadherin and Vimeutin during hypoxia on MCF-7. MTT was used to study the effects of viability.Transwell chamber was used to detect the ability of invasion and metastasis. Results The expression of E-cadherin was significantly lower (0.09±0.02)(t=30.98,P=0.0007) and the expression of Vimentin was significantly higher (0.69±0.04) (t=915,P=0.0000) with the extension of hypoxia.The capability of adhesion (81.23±0.74) (t=82.05,P=0.000),invasion(120±6) (t=22.78,P=0.0009) and migration(190±6) (t=23.49,P=0.000)was significantly increased after 72 h hypoxia(P＜0.05).Conclusion Hypoxia can downregulate E-cadherin and upregulate Vimentin and enhance the adhesion,invasion and migration of MCF-7.
