目的

探讨口腔黏膜白斑（OLK）组织基因表达谱的变化及相关信号通路的改变。

方法

采用Affymetrix U133 plus 2.0 基因芯片检测OLK 和正常口腔黏膜差异表达基因；采用GO 分析和Pathway 分析等生物信息学方法进一步了解相关信号通路的改变。

结果

OLK和正常黏膜组织相比存在682 个差异表达基因，其中645 个表达上调、37 个表达下调。Pathway分析显示黏着斑通路、过氧化物酶体增殖物激活受体通路、胰岛素信号通路、紧密连接、糖原异生、脂肪细胞因子通路、细胞骨架肌动蛋白调节等通路变化较显著，其中黏着斑（Focal adhesion）通路变化最显著，该通路中的MYLPF、ACTN2、MYLK3、CAV3、IGF-1、COL11A1 基因表达均有显著变化，提示Focal adhesion 通路可能参与了白斑的发生发展。

结论

OLK 的发生是一个多基因改变、多条信号通路协同作用的过程；黏着斑通路异常可能与白斑的发生密切相关。

Objective

To evaluate differentially expressed genes and the changes of associated pathways in the development of oral leukoplakia （OLK）.

Methods

The differentially expressed genes of OLK and normal oral mucosa were screened by human genome Affymetrix U133 plus 2.0 Array.The results were further analyzed by bioinformatics software including Gene Ontology analysis and pathway analysis to explore the changes of associated pathways.

Results

An oligonucleotide microassay analysis revealed significant changes in the expression of 682 genes， including 645 up-regulated genes and 37 down-regulated genes between oral leukoplakia and normal oral mucosa.The pathway analysis suggested that several pathways significantly changed， such as Focal adhesion pathway， PPAR signaling pathway， insulin signaling pathway，tight junction， glycolysis/gluconeogenesis， adipocytokine signaling pathway and regulation of actin cytoskeleton.The most significantly changed pathway was Focal adhesion pathway.These genes including MYLPF， ACTN2， MYLK3， CAV3， IGF-1 and COL11A1 were significantly changed in Focal adhesion pathway， suggesting that Focal adhesion pathway may involve in the development of OLK.

Conclusions

Multi-genes changes and multiple signaling pathways play synergistic roles in the progression of OLK.The abnormality of Focal adhesion pathway may be significantly associated with OLK.