摘要
目的:探明STAT3在肺腺癌细胞中增殖分化、抗凋亡作用与耐药之间的关系。方法:2003-09/2004-01在第三军医大学,采用浓度梯度递增法诱导A549形成耐药细胞系,免疫组化及蛋白印迹法联合检测A549及耐药株中STAT3,肺耐药蛋白,多药耐药蛋白表达情况。结果:成功诱导了A549/CARP耐药细胞株。免疫组化:A549组,A549/CARP组STAT3阳性细胞数差异无显著性意义(146.53±23.41和166.73±43.06,t=1.519,P>0.05);肺耐药蛋白(119.93±42.10和172.67±44.89,t=3.350)和多药耐药蛋白(112.40±35.07和151.73±33.92,t=3.747)阳性细胞数差异有显著性意义(P<0.01);STAT3,肺耐药蛋白,多药耐药蛋白之间表达均无相关性意义(P>0.05)。蛋白印迹:A549组,A549/CARP组均存在STAT3蛋白的表达,二者差异无显著性意义(P>0.05);STAT3,肺耐药蛋白,多药耐药蛋白之间表达均无相关性(P>0.05)。结论:STAT3参与了肺腺癌的增殖分化和抗凋亡作用,并未参与介导肺腺癌的耐药;肺耐药蛋白和多药耐药蛋白均参与了诱导肺腺癌的耐药,但二者之间无相关性;肺耐药蛋白和多药耐药蛋白介导的耐药机制与STAT3信号传导途径无关;可通过破坏STAT3信号传导来控制肿瘤细胞的生长和增殖,为肺癌的治疗提供以STAT3为靶向的基因治疗。
AIM:To elucidate the relationship of signal transducer and activator of transc ription 3(STAT3) in proliferation and differentiation,anti apoptosis and drug r esistance of lung adenocarcinoma. METHODS:In Third Military Medical University of Chinese PLA from September 200 3 to January 2004,CARP resistant A549(A549/CARP) was developed by increasing co ncentration gradient progressively.Immunohistoc hemical and Western blotting detection were used to detect STAT3,lung resista nce related protein(LRP) and multiple resistance protein(MRP) in A549 and A549/ CARP. RESULTS:Resistant subline A549/CARP was induced successfully.By immunohistoche mistry:There was no significant difference in the positive cells of STAT3 betwee n A549 group and A549/CARP group(146.53±23.41 vs 166.73±43.06,t=1.519,P >0.05) .But,there was significant difference between A549 group and A549/CARP group in the positive cells of LRP(119.93±42.10 vs 172.67±44.89,t=3.350) and MRP(112.40 ±35.07 vs 151.73±33.92,t=3.747)(both P< 0.01).The expression of STAT3 is not c orrelated with that of LRP and MRP(P >0.05).By Western blotting:There was no si gnificant difference in the expression of STAT3 between A549 group and A549/CARP group(P >0.05).The expression of STAT3 is not correlated with that of LRP and M RP(P >0.05). CONCLUSION:It is suggested that STAT3 plays a positive role in hyperplasia,dif ferentiation and anti apoptosis,but not in drug resistance.LRP and MRP may play a positive role in drug resistance of lung adenocarcinoma,but no correlation is found between them.The drug resistant mechanism of LRP and MRP is not correlate d with the signal transduction pathway of STAT3.It is feasible to destroy signal transduction pathway of STAT3 to inhibit the growth and proliferation of adenoc arcinoma cells,which will contribute to the targeting gene therapy using STAT3 f or lung adenocarcinoma.
出处
《中国临床康复》
CSCD
北大核心
2005年第14期128-129,i006,共3页
Chinese Journal of Clinical Rehabilitation
基金
四川省科技厅重点课题(03JY029-009)~~
