STAT3、MRP、LRP在肺腺癌A549及A549/CARP耐卡铂细胞株中的表达及关系的研究

THE RESEARCH OF THE EXPRESSION AND RELATIONSHIP OF STAT3、MRP、LRP IN LUNG ADENOCARCINOMA A549 AND CARP-RESISTANT A549(A549/CARP)

目的:探明STAT3与肺腺癌细胞多药耐药之间的关系。方法:采用免疫组化法测定A549及A549/CARP耐卡铂细胞株中STAT3、LRP、MRP蛋白表达情况。结果:STAT3在A549组、A549/CARP组中阳性细胞数无显著性差异(t=1.519,P>0.05);LRP、MRP在A549组、A549/CARP组中阳性细胞数有显著性差异(t=3.350,P<0.01)(t=3.747,P<0.01);STAT3、LRP、MRP之间表达均无相关性(r=0.061,P>0.05)。结论:STAT3并未直接参与介导肺腺癌的多药耐药性;LRP、MRP均参与了诱导肺腺癌的耐药,但二者之间无相关性;STAT3信号传导途径与LRP、MRP蛋白的激活机制可能无关。

Objective： To elucidate the relationship of signal transducer and activator of transcription 3 with multiple resistance of lung adenocarcinoma. Methods： Immunohistochemistry was taken to measure protein expression of STAT3,MRP,LRP in lung adenocaroinoma A549 and CARP-resistant A549（A549/CARP）. Results： There was no significant difference in the expression of STAT3 in A549 and A549/CARP （t=1.159,P〉0.05）. There was signifcant difference in the expression of LRP and MRP between A549 and A549/CARP （t=3.350,P〈0.01） （t=3.747,P〈0.01）. The expression of STAT3 was not correlated with LRP and MRP （t=0.061,P〉0.05）. Conclusion： It is suggested that STAT3 does not play a direct role in multiple resistance.The overexpression of LRP and MRP in drug-resistance cell and low expression in adenocarcinoma may play a positive role in drug resistance. The drug resistant mechanism of LRP and MRP was not correlated with the pathway of STAT3.