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AIM:Osteopontin (OPN) is a phosphorylated glycoproteinwith diverse functions including cancer development,progression and metastasis.It is unclear how osteopontinis regulated in HepG2 cells.The aim of this study was toinvestigate the effect of epidermal growth factor on theexpression of osteopontin in HepG2 cells,and to explorethe signal transduction pathway mediated this expression.METHODS:Osteopontin expression was detected by RNAaseprotection assay and Western blot.Wortmannin,a specificinhibitor of PI3K,was used to see if PI3K signal transductionwas involved in the induction of osteopontin gene expression.RESULTS:HepG2 cells constitutively expressed low levelsof osteopontin.Treatment with epidermal growth factorincreased osteopontin mRNA and protein level in a dose-and time-dependent manner.Application of wortmannincaused a dramatic reduction of epidermal growth factor-induced osteopontin expression.CONCLUSION:Osteopontin gene expression can be inducedby treatment of HepG2 cells with epidermal growth factor.Epidermal growth factor may regulate osteopontin geneexpression through PI3K signaling pathway.Several potentialtargets in the pathway can be manipulated to block thesynthesis of osteopontin and inhibit liver cancer metastasis.
AIM: Osteopontin (OPN) is a phosphorylated glycoprotein with diverse functions including cancer development, progression and metastasis. It is unclear how osteopontinis regulated in HepG2 cells. The AIM of this study was to investigate the effect of epidermal growth factor on the expression of osteopontin in HepG2 cells , and to explore the signal transduction pathway mediated this expression. METHODS: Osteopontin expression was detected by RNAase detection assay and Western blot. Wortmannin, a specific inhibitor of PI3K, was used to see if PI3K signal transduction was involved in the induction of osteopontin gene expression .RESULTS: HepG2 cells constitutively expressed low levels of osteopontin. Treatment with epidermal growth factor in creased osteopontin mRNA and protein level in a dose-and time-dependent manner. Application of wortmannincaused a dramatic reduction of epidermal growth factor-induced osteopontin expression. CONCLUSION: Osteopontin gene expression can be inducedby treatment of HepG2 cells wit h epidermal growth factor. Epidermal growth factor may regulate osteopontin gene expression through PI3K signaling pathway. Seral potentialtargets in the pathway can be manipulated to block thesynthesis of osteopontin and inhibit liver cancer metastasis.