CA916798基因通过PI3K/AKT通路参与肺癌顺铂耐药  

CA916798 gene is involved in cisplatin resistance in human lung cancer through PI3K/AKT pathway

作　　者：祝冰晶[1] 王宇亮[1] 罗虎[1] 周向东[1] 

机构地区：[1]第三军医大学西南医院呼吸内科,重庆400038

出　　处：《第三军医大学学报》2013年第7期618-621,共4页Journal of Third Military Medical University

基　　金：国家自然科学基金(30971308)~~

摘　　要：目的在前期体外研究的基础上,建立裸鼠移植瘤模型,观察阻断PI3K/AKT通路对肺腺癌细胞A549及多药耐药肺腺癌细胞A549/CDDP内CA916798基因mRNA表达的影响。方法建立A549、A549/CDDP裸鼠移植瘤模型,以LY294002作用A549组和A549/CDDP组后,比较各组移植瘤生长情况,HE染色观察组织结构变化,实时荧光定量PCR检测肿瘤细胞中CA916798基因mRNA的表达水平。结果成功建立裸鼠移植瘤模型,以LY294002分别阻断A549、A549/CDDP组裸鼠移植瘤细胞的PI3K/AKT通路后,移植瘤体积明显缩小,CA916798基因的表达明显下调(P<0.05)。结论抑制PI3K/AKT通路能够明显抑制肺腺癌细胞A549及A549/CDDP的恶性增殖。Objective To determine the effect of blocking the PI3K/AKT pathway on the expression of CA916798 gene in nude mouse transplanted tumor of human lung adenocarcinoma cell line A549 and the multidrug-resistant cell line A549/CDDP. Methods A total of 20 nude mice were randomly and equally divided into 4 groups, that is, A549, A549/CDDP, A549 ＋ LY294002, and A549/CDDP ＋ LY294002 groups. The animal model with A549 cells and A549/CDDP cells transplanted tumor was established in these corre- sponding nude mice. LY294002 of 25 mg/kg was treated in the mice of the 2 later groups. The size of tumor was measured, and morphology of the mass was observed after HE staining. Real-time fluorescent quantitative PCR was performed to detect CA916798 mRNA expression in the tumor. Results The model of transplanted tumor was established in nude mice successfully. Blocking PI3K/AKT pathway with LY294002 resulted in significantly decreased expression of CA916798 at mRNA level （ P 〈 0.05 ）, and reduced tumor volume. Conclusion Inhibition of PI3K/AKT pathway significantly inhibits the malignant proliferation in lung adeno- carcinoma cell A549 and muhidrug-resistant cell line A549/CDDP.

关 键 词：CA916798 耐药 顺铂 PI3K/AKT 

分 类 号：R73-361[医药卫生—肿瘤] R734.2[医药卫生—临床医学]