论文摘要
目的（1）观察血管性血友病因子（von Willnbrang factor,vWF）与整合素β3（integrinβ3）在不同转移潜能人肺癌细胞H460及GLC-82的表达,探讨vWF及integrinβ3与人肺癌转移的关系。（2）观察vWF与不同转移潜能人肺癌细胞H460及GLC-82黏附的关系,探讨vWF黏附与人肺癌转移的相关性。（3）探讨在人肺癌细胞H460及GLC-82 vWF与integrinβ3之间的相互关系。方法（1）应用免疫组化技术观察vWF及integrinβ3分别在不同转移潜能人肺癌细胞H460及GLC-82的表达。（2）应用vWF黏附试验及MTT法观察vWF分别与不同转移潜能人肺癌细胞H460及GLC-82黏附的关系（3）联合应用vWF黏附试验、抗体抑制试验及MTT法,观察vWF与integrinβ3之间的相互关系。结果（1）免疫组化结果显示在转移性较高的人肺癌细胞H460 integrinβ3和vWF的表达呈强阳性,在转移性较低的人肺癌细胞GLC-82 integrinβ3和vWF的表达呈弱阳性。（2）用anti-vWF抑制后人肺癌细胞H460及GLC-82 integrinβ3的表达强度无明显变化,用anti-integrinβ3抑制后人肺癌细胞H460及GLC-82 vWF的表达强度无明显变化。（3）vWF可以和人肺癌细胞H460及GLC-82黏附,当从0.5μg·ml-1、1.0μg·ml-1到2.0μg·ml-1逐渐增加vWF浓度时,MTT法测得vWF与H460及GLC-82细胞黏附A值逐渐增加,呈剂量依赖性,到2.0μg·ml-1后再增加vWF浓度,A值不再增加。（4）Anti-integrinβ3抑制后vWF与H460细胞黏附降低,当逐渐增加anti-integrinβ3浓度从70μg·ml-1、75μg·ml-1、80μg·ml-1到85μg·ml-1时,MTT法测得vWF与H460细胞黏附A值由1.5923±0.0561逐渐降到0.5507±0.0309,P=0.01619。Anti-vWF抑制后这种黏附也降低,当逐渐增加anti-vWF浓度从1.0μg·ml-1、1.5μg·ml-1到2.0μg·ml-1时,MTT法测得vWF与H460细胞黏附A值由1.6023±0.0601逐渐降到0.5380±0.0340,P=0.01598。两种抗体抑制黏附差异无显著性。（5）Anti-integrinβ3抑制后vWF与GLC-82细胞黏附降低,当逐渐增加anti-integrinβ3浓度从70μg·ml-1、75μg·ml-1到80μg·ml-1时,MTT法测得vWF与GLC-82细胞黏附A值由1.3969±0.0480逐渐降到0.3887±0.0237,P=0.01519。Anti-vWF抑制后vWF与人肺癌细胞GLC-82的黏附也降低,当逐渐增加anti-vWF浓度从1.0μg·ml-1到1.5μg·ml-1时,MTT法测得vWF与GLC-82细胞黏附A值由1.3968±0.0490逐渐降到0.3510±0.0271,P=0.01609。两种抗体抑制黏附差异无显著性。结论（1）vWF及integrinβ3在转移性较高的人肺癌细胞H460表达呈强阳性,而在转移性较低的人肺癌细胞GLC-82表达呈弱阳性,提示vWF及integrinβ3与人肺癌转移可能呈正相关。（2）vWF能与人肺癌细胞H460及GLC-82黏附,且与较高转移性的人肺癌细胞H460黏附较强,表明vWF通过与人肺癌胞H460及GLC-82黏附促进其转移。（3）Anti-integrinβ3及anti-vWF两种抗体可以抑制vWF与人肺癌细胞H460及GLC-82的黏附,抑制黏附的效果相同,提示vWF可能与integrinβ3结合发挥作用。
论文目录
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