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目的:本研究探讨Toll样受体4(toll-like receptor4,TLR4)介导的信号转导通路在脂多糖(lipopolysaccharide,LPS)促进肺腺癌细胞A549增殖过程中的可能机制。方法:LPS刺激肺腺癌A549细胞后,采用MTT方法和FCM法检测A549细胞增殖情况;免疫细胞化学法检测经不同浓度LPS处理的A549细胞中,TLR4、c-Jun、c-Fos及核因子-κB(nuclear factor-kappa B,NF-κB)蛋白的表达水平。结果:LPS刺激A549细胞24 h后增殖效应最明显,且100 ng/mL LPS组的G2/M期细胞所占比例较对照组和10 ng/mL LPS组显著增加,差异有统计学意义(P<0.05)。TLR4、c-Jun、c-Fos及NF-κB蛋白在A549细胞中均有表达,且随着LPS处理浓度的增加而表达增强,100 ng/mL LPS处理组中蛋白表达增强最明显,与对照组比较差异有统计学意义(P<0.05)。结论:LPS能促进A549细胞增殖,其机制可能是通过与TLR4受体结合而激活TLR4信号转导通路,进而分别活化c-Jun和c-Fos的异源二聚体———转录因子激活蛋白-1(activating protein-1,AP-1)和核因子NF-κB,从而使肺癌细胞持续增殖。
AIM: To investigate the possible mechanism of toll-like receptor 4 (TLR4) -mediated signal transduction pathway in the proliferation of lung adenocarcinoma A549 cells induced by lipopolysaccharide (LPS). Methods: The proliferation of A549 cells was detected by MTT assay and FCM assay after A549 cells were stimulated by LPS. The expressions of TLR4, c-Jun, c-Fos and NF-κB in A549 cells treated with different concentrations of LPS were detected by immunocytochemistry -κB (nuclear factor-kappa B, NF-κB) protein expression levels. RESULTS: The proliferation of A549 cells was the most obvious after 24 h stimulation with LPS, and the proportion of G2 / M phase cells in 100 ng / mL LPS group was significantly increased compared with that in control group and 10 ng / mL LPS group (P <0.05). The expression of TLR4, c-Jun, c-Fos and NF-κB protein in A549 cells were both increased with the increase of LPS concentration. The expression of TLR4, c-Jun, The difference was statistically significant (P <0.05). CONCLUSION: LPS can promote the proliferation of A549 cells by activating the TLR4 signal transduction pathway by binding to TLR4 receptor, which in turn activates the heterodimers of c-Jun and c-Fos, the transcription factor activator protein 1 (activating protein-1, AP-1) and nuclear factor NF-κB, so that lung cancer cells continue to proliferate.