轉錄活化Pentraxin3基因表現與表皮生長因子誘導頭頸癌細胞轉移具有相關性

吳碩倫

doi:10.6844/NCKU.2014.01754

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轉錄活化Pentraxin3基因表現與表皮生長因子誘導頭頸癌細胞轉移具有相關性

Transcriptional activation of pentraxin-3 gene expression is associated with EGF-induced head and neck cancer cell metastasis

吳碩倫 , Masters　　Advisor：陳炳焜　　

繁體中文 DOI： 10.6844/NCKU.2014.01754

頭頸癌；表皮生長因子； PTX3 ；癌症轉移； Head and neck cancer ； epidermal growth factor ； PTX3 ； metastasis

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SUMMARY

Overexpression of epidermal growth factor receptor (EGFR) and production of proinflammatroy cytokines are well clarified in head and neck squamous cell carcinoma (HNSCC) and correlates with invasion and metastasis. However, molecular mechanisms by which EGFR-mediated cytokines regulates metastasis of HNSCC remain unclear. Here, we identified that PTX3 is a metastasis-promoting factor that mediate EGF-induced HNSCC metastasis. Analysis of PTX3 expression between normal and malignant or metastatic tissues from HNSCC patients by using published datasets, our results indicated that expression level of PTX3 in malignant tissues was higher than in normal part in HNSCC patients. In addition, we found that EGF induced transcriptional activation of PTX3 by activating the binding of c-Jun and NF-κB factors to AP-1/NF-κB binding site of the PTX3 promoter. PI3K/AKT and NF-κB were essential for the induction of PTX3. EGF-induced PTX3 expression was significantly inhibited in c-Jun and NF-κB knockdown cells. Furthermore, we identify that NF-κB is upstream regulator to c-Jun in EGF signaling pathway. EGF stimulated the secretion of PTX3 from cancer cell, resulting in enhancing cell migration, local invasion, attachment with endothelium and distal dissemination. Effects of EGF on the induction of fibronectin and MMP9 expression, and inhibition of E-cadherin were abolished in PTX3 knockdown cells. These findings reveal the mechanism that autocrine production of EGF-induce PTX3-regulated HNSCC metastasis was through enhancing metastatic molecules, such as fibronectin and MMP9 expression. Induction of PTX3 possibly reflecting the EGFR-caused HNSCC metastasis associated with inflammation.

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