摘要
目的:探讨瘦素在促进肺癌细胞增殖过程中的可能机制,并探讨其在肺癌发生发展中的作用。方法:MTT法检测瘦素对肺癌A549细胞的促增殖作用。流式细胞术检测不同浓度瘦素处理组肺癌A549细胞的增殖率。免疫细胞化学法检测经不同浓度瘦素处理的A549细胞中STAT3、p-STAT3及Bcl-2蛋白的表达。结果:STAT3、p-STAT3及Bcl-2蛋白在A549细胞中均有表达。瘦素处理后的A549细胞中STAT3、p-STAT3及Bcl-2的表达随着处理浓度增加而增强,且100ng/mL瘦素处理组表达增加最明显,与对照组比较差异有显著性(P<0.05);瘦素刺激A549细胞24h后增殖效应最明显,且100ng/mL组G2/M期细胞所占的比例较对照组和10ng/mL组显著增加(P<0.05)。结论:瘦素可能通过JAK/STAT3通路,活化STAT3介导抗凋亡基因Bcl-2的过度表达而使肺癌细胞呈持续增殖。
Objective To study the mechanism of leptin in stimulating the proliferation of human lung adenocarcinoma cells, and to investigate its function in the development of human lung cancer. Methods The proliferation stimulating effect of leptin on lung cancer A549 cells was determined by MTT assay. The growth rates of A549 cells treated by different concentrations of leptin were detected by flow cytometry. The expressions of the protein of STAT3, p-STAT3, and Bcl-2 in A549 ceils were evaluated by immunocytochemistry staining. Results The expressions of the protein of STAT3, p-STAT3, and Bcl-2 in A549 cells were observed, and were gradually increased with the time and concentration of leptin increased, and reached their peak in 100 ng/mL leptin group, which were significantly different from those in control group （P 〈 0.05）. Leptin can stimulate the proliferation of A549 cells, especially when leptin was 100 ng/mL after 24-hour treatment. Moreover, the ratio of cells in G2/M cell cycle in those treated with 100 ng/mL leptin was significantly higher than those in 0 and 10 ng/mL leptin treated group （P 〈 0.05）. Conclusion Leptin may promote the proliferation of A549 cells by activating STAT3 signaling pathway and inducing the over expression of Bcl-2.
出处
《实用医学杂志》
CAS
北大核心
2009年第19期3184-3187,共4页
The Journal of Practical Medicine
基金
安徽省自然科学基金资助项目(编号:070413068)
