Guo-Xin Zhang1, Zhi-Quan Zhao, Hong-Di Wang, Bo Hao. 1. Department of Gastroenterology, the First Affiliated Hospital, Nanjing Medical University, Nanjing 210029, Jiangsu Province, China. guoxinz2002@yahoo.com
Abstract
AIM: Osteopontin (OPN) is a phosphorylated glycoprotein with diverse functions including cancer development, progression and metastasis. It is unclear how osteopontin is 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 protection 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 increased osteopontin mRNA and protein level in a dose- and time-dependent manner. Application of wortmannin caused a dramatic reduction of epidermal growth factor-induced osteopontin expression. CONCLUSION: Osteopontin gene expression can be induced by treatment of HepG2 cells with epidermal growth factor. Epidermal growth factor may regulate osteopontin gene expression through PI3K signaling pathway. Several potential targets in the pathway can be manipulated to block the synthesis 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 osteopontin is 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 protection 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 increased osteopontin mRNA and protein level in a dose- and time-dependent manner. Application of wortmannin caused a dramatic reduction of epidermal growth factor-induced osteopontin expression. CONCLUSION:Osteopontin gene expression can be induced by treatment of HepG2 cells with epidermal growth factor. Epidermal growth factor may regulate osteopontin gene expression through PI3K signaling pathway. Several potential targets in the pathway can be manipulated to block the synthesis of osteopontin and inhibit liver cancer metastasis.
Authors: Jae-Hoon Kim; Steven J Skates; Toshimitsu Uede; Kwong-kwok Wong; John O Schorge; Colleen M Feltmate; Ross S Berkowitz; Daniel W Cramer; Samuel C Mok Journal: JAMA Date: 2002-04-03 Impact factor: 56.272
Authors: Zekuan Xu; Yi Zhang; Jiakai Jiang; Yang Yang; Ruihua Shi; Bo Hao; Zhihong Zhang; Zuhu Huang; Jin W Kim; Guoxin Zhang Journal: BMC Cancer Date: 2010-04-27 Impact factor: 4.430
Authors: K Matušan-Ilijaš; G Damante; D Fabbro; G Dorđević; I Hadžisejdić; M Grahovac; M Avirović; B Grahovac; N Jonjić; K Lučin Journal: Clin Transl Oncol Date: 2012-07-24 Impact factor: 3.405
Authors: Carolin Neumann; Fabian Garreis; Friedrich Paulsen; Christian M Hammer; Marco T Birke; Michael Scholz Journal: PLoS One Date: 2014-04-09 Impact factor: 3.240