title: Gallic acid suppresses cell viability, proliferation, invasion and angiogenesis in human glioma cells.
abstract: Gallic acid, an organic acid, also known as 3,4,5-trihydroxybenzoic acid, is cytotoxic against certain cancer cells, without harming normal cells. The objective of this study is to evaluate whether gallic acid can inhibit glioma cell viability, proliferation, invasion and reduce glioma cell mediated angiogenesis. Treatment of U87 and U251n glioma cells with gallic acid inhibited cell viability in a dose-dependent manner. BrdU and tube formation assays indicated that gallic acid significantly decreased glioma cell proliferation and tube formation in mouse brain endothelial cells, respectively. In addition, gallic acid decreased U87 cell invasion in vitro. Western blot analysis showed that expression of ADAM17, p-Akt and p-Erk was suppressed by gallic acid in both U87 and U251n cell lines. These data suggest that suppression of ADAM17 and downregulation of PI3K/Akt and Ras/MAPK signaling pathways may contribute to gallic acid-induced decrease of invasiveness. Gallic acid may be a valuable candidate for treatment of brain tumor.
authors.affiliation: Department of Health Technology and Informatics, The Hong Kong Polytechnic University, Hong Kong S.A.R., People's Republic of China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Lu
authors.forename: Feng
authors.initials: F
authors.lastname: Jiang
authors.forename: Hao
authors.initials: H
authors.lastname: Jiang
authors.forename: Kalina
authors.initials: K
authors.lastname: Wu
authors.forename: Xuguang
authors.initials: X
authors.lastname: Zheng
authors.forename: Yizhong
authors.initials: Y
authors.lastname: Cai
authors.forename: Mark
authors.initials: M
authors.lastname: Katakowski
authors.forename: Michael
authors.initials: M
authors.lastname: Chopp
authors.forename: Shing-Shun Tony
authors.initials: SS
authors.lastname: To
mesh_terms: D000818:Animals; D015153:Blotting, Western; D001932:Brain Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D002460:Cell Line; D045744:Cell Line, Tumor; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000235:genetics; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D042783:Endothelial Cells / Q000378:metabolism / Q000473:pathology; D005707:Gallic Acid / Q000378:metabolism* / Q000494:pharmacology; D005910:Glioma / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D051379:Mice; D009369:Neoplasms / Q000473:pathology*; D009389:Neovascularization, Pathologic / Q000378:metabolism; D051057:Proto-Oncogene Proteins c-akt / Q000235:genetics / Q000378:metabolism
chemical_list: D005707:Gallic Acid; D051057:Proto-Oncogene Proteins c-akt