| http://purl.uniprot.org/citations/27665471 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/27665471 | http://www.w3.org/2000/01/rdf-schema#comment | "Prostate cancer (PC) is one of the most common cancers among men. Progression of prostate cancer is associated with an increase in cellular level of interleukin-6 (IL-6). Gallic acid (GA) is a polyhydroxy phenolic compound which can inhibit the growth of cancer cells. The aim of this study was to evaluate the effects of GA treatment on cell viability, proliferation, invasion, IL-6 gene expression, IL-6 secretion, cellular levels of pSTAT3, pERK1/2, and pAKT signaling proteins in human prostate cancer PC3 cells. PC3 cells viability after treatment with GA (0-120μM) was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression of IL-6 was investigated using real-time polymerase chain reaction. Cellular concentration of pSTAT3, pERK1/2, and pAKT signaling proteins were determined by Western blotting technic. PC3 cells invasion was assessed by invasion assay test. Treatment with GA caused a significant decrease in cell viability, proliferation, invasion, cellular levels of pSTAT3, pERK1/2, and pAKT signaling proteins after 48h in a dose-dependent manner. The level of IL-6 and its gene expression decreased significantly in PC3 cells treated with GA. Our results show that IL-6 down-regulation and decreased IL-6 protein level in PC3 cells by GA resulted in diminishing of pSTAT3, pERK1/2, and pAKT signaling proteins which lead to the reduction of the cell survival, proliferation, and invasion in PC3 cells. Therefore, it seems that GA can be considered an anticancer agent in the treatment of prostate cancer."xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.org/dc/terms/identifier | "doi:10.1016/j.biopha.2016.09.046"xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/author | "Ghatreh-Samani K."xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/author | "Heidarian E."xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/author | "Keloushadi M."xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/author | "Valipour P."xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/date | "2016"xsd:gYear |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/name | "Biomed Pharmacother"xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/pages | "264-269"xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/title | "The reduction of IL-6 gene expression, pAKT, pERK1/2, pSTAT3 signaling pathways and invasion activity by gallic acid in prostate cancer PC3 cells."xsd:string |
| http://purl.uniprot.org/citations/27665471 | http://purl.uniprot.org/core/volume | "84"xsd:string |
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