| Summary: | 碩士 === 國立成功大學 === 生物資訊與訊息傳遞研究所 === 100 === PTX3 belongs to the pentraxin superfamily, is induced by pro-inflammatory factors such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNFα), and lipopolysaccharide (LPS), and is involved in immunity, matrix remodeling, angiogenesis, fertility and apoptosis. Previous reports have shown that overexpression of PTX3 was found in the soft tissue liposarcoma and up-regulation of PTX3 had highly correlation with overexpression of epidermal growth factor receptor (EGFR) in the prostate cancer. However, the mechanism involved in EGF-regulated PTX3 expression is not clear. The aim of this study is to characterize whether EGF can induce PTX3 expression and to investigate the functional role of PTX3 in the tumor microenvironment. In the present study, we used RT-PCR, western blotting and ELISA to clarify that EGF-induced the expression of PTX3 was in a time-dependent manner in cancer cells. We used actinomycin D treatment and reporter assay to clarify EGF induces the expression of PTX3 through transcriptional activation or stabilizing mRNA. We silenced genes that are downstream of EGFR-signaling pathway by lentiviral vector-derived shRNAs and found that EGF induced the expression of PTX3 through EGFR-related downstream pathways. In functional assay, PTX3 is involved in EGF-regulated cell function. These results suggested that EGF-induced PTX3 expression was through EGFR pathway, resulting in the regulation of cell function.
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