title: Gallic acid inhibits gastric cancer cells metastasis and invasive growth via increased expression of RhoB, downregulation of AKT/small GTPase signals and inhibition of NF-κB activity.
abstract: Our previous study demonstrated the therapeutic potential of gallic acid (GA) for controlling tumor metastasis through its inhibitory effect on the motility of AGS cells. A noteworthy finding in our previous experiment was increased RhoB expression in GA-treated cells. The aim of this study was to evaluate the role of RhoB expression on the inhibitory effects of GA on AGS cells. By applying the transfection of RhoB siRNA into AGS cells and an animal model, we tested the effect of GA on inhibition of tumor growth and RhoB expression. The results confirmed that RhoB-siRNA transfection induced GA to inhibit AGS cells' invasive growth involving blocking the AKT/small GTPase signals pathway and inhibition of NF-κB activity. Finally, we evaluated the effect of GA on AGS cell metastasis by colonization of tumor cells in nude mice. It showed GA inhibited tumor cells growth via the expression of RhoB. These data support the inhibitory effect of GA which was shown to inhibit gastric cancer cell metastasis and invasive growth via increased expression of RhoB, downregulation of AKT/small GTPase signals and inhibition of NF-κB activity. Thus, GA might be a potential agent in treating gastric cancer.
authors.affiliation: Institute of Biochemistry and Biotechnology, Chung Shan Medical University, Taichung 402, Taiwan.
authors.forename: Hsieh-Hsun
authors.initials: HH
authors.lastname: Ho
authors.forename: Chi-Sen
authors.initials: CS
authors.lastname: Chang
authors.forename: Wei-Chi
authors.initials: WC
authors.lastname: Ho
authors.forename: Sheng-You
authors.initials: SY
authors.lastname: Liao
authors.forename: Wea-Lung
authors.initials: WL
authors.lastname: Lin
authors.forename: Chau-Jong
authors.initials: CJ
authors.lastname: Wang
mesh_terms: D000818:Animals; D045744:Cell Line, Tumor; D015536:Down-Regulation / Q000187:drug effects / Q000502:physiology; D020558:GTP Phosphohydrolases / Q000378:metabolism*; D005707:Gallic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D009361:Neoplasm Invasiveness / Q000473:pathology / Q000517:prevention & control; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology; D013274:Stomach Neoplasms / Q000378:metabolism*; D020743:rhoB GTP-Binding Protein / Q000096:biosynthesis*
chemical_list: D016328:NF-kappa B; D005707:Gallic Acid; D051057:Proto-Oncogene Proteins c-akt; D020558:GTP Phosphohydrolases; D020743:rhoB GTP-Binding Protein