李振宇1 李月旺2 王廷杰1 金巴特尔1 张志刚1.内毒素诱导非小细胞肺癌细胞增殖及其机制
李[J].现代生物医学进展英文版,2014,14(8):1449-1551. |
内毒素诱导非小细胞肺癌细胞增殖及其机制
李 |
Effects of Endotoxin on Tumor Proliferation in the Non-Small CellLung Cancer and Underlying Mechanisms |
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DOI: |
中文关键词: 肺癌 内毒素 肿瘤增殖 |
英文关键词: Lung cancer Endotoxin Tumor proliferation |
基金项目: |
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中文摘要: |
摘要目的:研究内毒素对体外培养非小细胞肺癌(NSCLC)细胞株A549 细胞增殖的影响及其机制。方法:不同浓度脂多糖(LPS)
进行8-48h 干预,MTT 及细胞计数法检测其对A549 细胞增殖的影响;EGFR中和抗体或COX-2 抑制剂与LPS联合干预,检测其
对A549 细胞增殖及PGE2 的影响。结果:LPS 可引发A549 细胞MTT 活性和细胞计数显著增加,且呈现时间和剂量依赖性。LPS
还可诱发PGE2 水平显著升高。药物干预结果显示,抑制COX-2 或EGFR 可明显逆转LPS 所引发的细胞增殖和PGE2 水平升高
趋势。结论:LPS 可能通过激活EGFR 和COX-2 信号途径,诱导体外培养的非小细胞肺癌细胞增殖分化。肺部感染可能会加速非
小细胞肺癌进展,并可能造成不良预后。 |
英文摘要: |
ABSTRACT Objective:To investigate the effect of endotoxin on tumor proliferation in the non-small cell lung cancer and the
underlying mechanisms. Methods:Different concentrations of Lipopolysaccharide (LPS) were intervented from 8 to 48 h. The effection
of LPS on the proliferation of A549 cells with MTT and cell counting were tested. The intervention effect of the combination of EGFR
neutralizing antibody or COX-2 inhibitors with LPS on the proliferation of A549 cells and PGE2 were tested. Results:LPS induced a
time- and dose-dependent increase in proliferation of A549 cells as quantified by MTS activity and cell counting. Large amounts of
COX-2-derived prostaglandin (PG) E2 were secreted from LPS-stimulated A549 cells. Pharmacological interventions revealed that
inhibition of COX-2 and EGFR activity in A549 cells severely attenuated both PGE2 release and proliferation in response to LPS.
Conclusion:LPS induces proliferation of NSCLC cells inhuman NSCLC specimen via EGFR- or COX-2-signaling. Pulmonary
infection may thus directly induce tumor progression in NSCLC. |
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