中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2014年
10期
1794-1799
,共6页
左蓓%刑敏%孙珍贵%汪向海%陈兴无
左蓓%刑敏%孫珍貴%汪嚮海%陳興無
좌배%형민%손진귀%왕향해%진흥무
缺氧%小窝蛋白-1%缺氧诱导因子1α%肺肿瘤
缺氧%小窩蛋白-1%缺氧誘導因子1α%肺腫瘤
결양%소와단백-1%결양유도인자1α%폐종류
Anoxia%Caveolin-1%Hypoxia-inducible factor-1α%Lung neoplasms
目的：探讨低氧诱导剂二氯化钴（CoCl2）对小窝蛋白-1（Cav-1）生成的调节作用及后者对人肺腺癌A549细胞迁移、侵袭的影响。方法：检测肺癌患者伴恶性胸水（ MPE）和结核性胸膜炎患者胸水（ TBPE）中Cav-1和缺氧诱导因子（ HIF）-1α浓度，比较两者相关性；以CoCl2和（或） HIF-1α抑制剂YC-1作用于A549细胞ELISA法检测细胞上清Cav-1和HIF-1α浓度；分别采用细胞划痕实验及Transwell小室侵袭实验研究CoCl2刺激表达的Cav-1对A549细胞迁移和侵袭的影响。结果：MPE中Cav-1和HIF-1α浓度明显高于TBPE，两组患者胸水中Cav-1与HIF-1α均呈正相关。 CoCl2浓度和时间依赖性诱导A549细胞Cav-1和HIF-1α生成，200μmol/L或24 h达到峰值；浓度＞200μmol/L或作用时间超过24 h则呈现浓度或时间依赖性抑制。 HIF-1α抑制剂YC-1浓度依赖性抑制HIF-1α和Cav-1生成。 CoCl2浓度依赖性增强A549细胞迁移和侵袭，200μmol/L作用最强；YC-1对上述过程产生抑制效应。结论：肺癌患者胸腔积液中Cav-1浓度升高，低氧诱导Cav-1生成的变化可能参与了A549细胞迁移和侵袭，HIF-1α可能对Cav-1生成发挥影响。
目的：探討低氧誘導劑二氯化鈷（CoCl2）對小窩蛋白-1（Cav-1）生成的調節作用及後者對人肺腺癌A549細胞遷移、侵襲的影響。方法：檢測肺癌患者伴噁性胸水（ MPE）和結覈性胸膜炎患者胸水（ TBPE）中Cav-1和缺氧誘導因子（ HIF）-1α濃度，比較兩者相關性；以CoCl2和（或） HIF-1α抑製劑YC-1作用于A549細胞ELISA法檢測細胞上清Cav-1和HIF-1α濃度；分彆採用細胞劃痕實驗及Transwell小室侵襲實驗研究CoCl2刺激錶達的Cav-1對A549細胞遷移和侵襲的影響。結果：MPE中Cav-1和HIF-1α濃度明顯高于TBPE，兩組患者胸水中Cav-1與HIF-1α均呈正相關。 CoCl2濃度和時間依賴性誘導A549細胞Cav-1和HIF-1α生成，200μmol/L或24 h達到峰值；濃度＞200μmol/L或作用時間超過24 h則呈現濃度或時間依賴性抑製。 HIF-1α抑製劑YC-1濃度依賴性抑製HIF-1α和Cav-1生成。 CoCl2濃度依賴性增彊A549細胞遷移和侵襲，200μmol/L作用最彊；YC-1對上述過程產生抑製效應。結論：肺癌患者胸腔積液中Cav-1濃度升高，低氧誘導Cav-1生成的變化可能參與瞭A549細胞遷移和侵襲，HIF-1α可能對Cav-1生成髮揮影響。
목적：탐토저양유도제이록화고（CoCl2）대소와단백-1（Cav-1）생성적조절작용급후자대인폐선암A549세포천이、침습적영향。방법：검측폐암환자반악성흉수（ MPE）화결핵성흉막염환자흉수（ TBPE）중Cav-1화결양유도인자（ HIF）-1α농도，비교량자상관성；이CoCl2화（혹） HIF-1α억제제YC-1작용우A549세포ELISA법검측세포상청Cav-1화HIF-1α농도；분별채용세포화흔실험급Transwell소실침습실험연구CoCl2자격표체적Cav-1대A549세포천이화침습적영향。결과：MPE중Cav-1화HIF-1α농도명현고우TBPE，량조환자흉수중Cav-1여HIF-1α균정정상관。 CoCl2농도화시간의뢰성유도A549세포Cav-1화HIF-1α생성，200μmol/L혹24 h체도봉치；농도＞200μmol/L혹작용시간초과24 h칙정현농도혹시간의뢰성억제。 HIF-1α억제제YC-1농도의뢰성억제HIF-1α화Cav-1생성。 CoCl2농도의뢰성증강A549세포천이화침습，200μmol/L작용최강；YC-1대상술과정산생억제효응。결론：폐암환자흉강적액중Cav-1농도승고，저양유도Cav-1생성적변화가능삼여료A549세포천이화침습，HIF-1α가능대Cav-1생성발휘영향。
AIM:To investigate the regulatory role of hypoxia mimic reagent cobalt chloride ( CoCl2 ) on cave-olin-1 (Cav-1) generation and the influence of Cav-1 on the abilities of migration and invasion of human lung adenocarcino-ma A549 cells.METHODS:The concentrations of Cav-1 and hypoxia-inducible factor ( HIF)-1αin pleural effusion of the patients with lung cancer ( MPE) or tuberculous pleurisy ( TBPE) were detected, and the correlation was also compared. A549 cells were treated with CoCl2 at different concentrations and time in the presence or absence of HIF-1αinhibitor YC-1.The concentrations of Cav-1 and HIF-1αin the cell supernatants were measured by ELISA.The effects of Cav-1 induced by CoCl2 on the migration and invasion of A549 cells were determined by scratch test and Transwell invasion trial, respec-tively.RESULTS:The levels of Cav-1 and HIF-1αin MPE were significantly higher than those in TBPE.There was a highly positive correlation between Cav-1 and HIF-1αlevels in the pleural effusion.CoCl2 induced the generation of Cav-1 and HIF-1αin A549 cells in a concentration-and time-dependent manner, the peak occurred at 200 μmol/L or 24 h, while the concentration over 200 μmol/L or after treated over 24 h, a concentration-or time-dependent inhibition was ob-served.HIF-1αinhibitor YC-1 concentration-dependently inhibited the generation of HIF-1αand Cav-1 induced by CoCl2 in A549 cells.CoCl2 enhanced A549 cells migration and invasion, with 200 μmol/L played the strongest role, which were down-regulated significantly in the presence of YC-1.CONCLUSION:The alteration of hypoxia-induced Cav-1 generation might be involved in the migration and invasion of A549 cells.A possible role for HIF-1αis indicated in Cav-1 generation.
