中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
20期
9194-9199
,共6页
谢成耀%高原%张秀伟%贺佳妮%郝凤霞%付琳%王晓荣%李庆昌
謝成耀%高原%張秀偉%賀佳妮%郝鳳霞%付琳%王曉榮%李慶昌
사성요%고원%장수위%하가니%학봉하%부림%왕효영%리경창
肺肿瘤%化疗耐药%GSK-3β
肺腫瘤%化療耐藥%GSK-3β
폐종류%화료내약%GSK-3β
Lung neoplasms%Chemotherapy resistance%GSK-3β
目的：研究人肺腺癌细胞系A549和其顺铂耐药细胞系A549/DDP中GSK-3β的磷酸化和胞内分布以探讨GSK-3β在顺铂耐药中的作用。方法蛋白质免疫印迹法检测A549/DDP和A549细胞质和细胞核中总GSK-3β、p-GSK-3βser9和p-GSK-3βtyr6的表达。MTT法、流式细胞术分别检测顺铂耐药性、肺癌细胞凋亡率。结果 A549/DDP细胞胞质中p-GSK-3βser9水平明显高于A549细胞（P＜0.01），顺铂的处理增加了A549/DDP细胞中p-GSK-3βser9的水平（P＜0.01），相反却减少了A549细胞中p-GSK-3βser9的水平（P＜0.01）。A549/DDP 细胞质中 p-GSK-3βtyr6水平明显低于 A549细胞（P＜0.01），顺铂的处理减少了A549/DDP细胞中p-GSK-3βtyr6的水平（P＜0.01），却增加了A549细胞中p-GSK-3βtyr6的水平（P＜0.01）。结论细胞质中GSK-3β活性受抑可能是非小细胞肺癌顺铂耐药的原因。
目的：研究人肺腺癌細胞繫A549和其順鉑耐藥細胞繫A549/DDP中GSK-3β的燐痠化和胞內分佈以探討GSK-3β在順鉑耐藥中的作用。方法蛋白質免疫印跡法檢測A549/DDP和A549細胞質和細胞覈中總GSK-3β、p-GSK-3βser9和p-GSK-3βtyr6的錶達。MTT法、流式細胞術分彆檢測順鉑耐藥性、肺癌細胞凋亡率。結果 A549/DDP細胞胞質中p-GSK-3βser9水平明顯高于A549細胞（P＜0.01），順鉑的處理增加瞭A549/DDP細胞中p-GSK-3βser9的水平（P＜0.01），相反卻減少瞭A549細胞中p-GSK-3βser9的水平（P＜0.01）。A549/DDP 細胞質中 p-GSK-3βtyr6水平明顯低于 A549細胞（P＜0.01），順鉑的處理減少瞭A549/DDP細胞中p-GSK-3βtyr6的水平（P＜0.01），卻增加瞭A549細胞中p-GSK-3βtyr6的水平（P＜0.01）。結論細胞質中GSK-3β活性受抑可能是非小細胞肺癌順鉑耐藥的原因。
목적：연구인폐선암세포계A549화기순박내약세포계A549/DDP중GSK-3β적린산화화포내분포이탐토GSK-3β재순박내약중적작용。방법단백질면역인적법검측A549/DDP화A549세포질화세포핵중총GSK-3β、p-GSK-3βser9화p-GSK-3βtyr6적표체。MTT법、류식세포술분별검측순박내약성、폐암세포조망솔。결과 A549/DDP세포포질중p-GSK-3βser9수평명현고우A549세포（P＜0.01），순박적처리증가료A549/DDP세포중p-GSK-3βser9적수평（P＜0.01），상반각감소료A549세포중p-GSK-3βser9적수평（P＜0.01）。A549/DDP 세포질중 p-GSK-3βtyr6수평명현저우 A549세포（P＜0.01），순박적처리감소료A549/DDP세포중p-GSK-3βtyr6적수평（P＜0.01），각증가료A549세포중p-GSK-3βtyr6적수평（P＜0.01）。결론세포질중GSK-3β활성수억가능시비소세포폐암순박내약적원인。
Objective To explore the role of GSK-3β in cisplatin resistance by evaluating the phosphorylation status and intracellular localization of GSK-3βin lung adenocarcinoma cell A549 and its cisplatin resistant cell clone A549/DDP. Methods Both total and nuclear/cytoplasmic GSK-3β, p-GSK-3βser9 and p-GSK-3βtyr6 expression were detected by Western blot. Cispatin resistance and cell apoptotic rate were measured by MTT and flow cytometry in both A549 and A549/DDP cells. Results Increased cytoplasmic p-GSK-3βser9 was observed in A549/DDP cells as compared to A549 cells(P<0.01). Cisplatin increased cytoplasmic p-GSK-3βser9 in A549/DDP cells but decreased it in A549 cells(P<0.01). Conversely, cytoplasmic levels of p-GSK-3βtyr216 were significantly decreased in A549/DDP cells as compared to A549 cells. The levels of p-GSK-3βtyr216 in the cytoplasm of A549/DDP cells decreased with cisplatin treatment while they increased in A549 cells(P<0.01). Conclusion Inhibition of cytoplasmic activity of GSK-3β was responsible for cisplatin resistance in lung adenocarcinoma.
