AGS Transfection Reagent (Gastic Adenocarcinoma, CRL 1739)

In the following study, researchers investigate the effect of low concentration hydrogen peroxide (H2O2) on the proliferation of AGS cells. AGS cells were treated with low concentrations of H2O2 for 48 hours. Methyl thiazolyl tetrazolium (MTT) method was used to analyze the effect of H2O2 concentration gradient on the activity of AGS cells. Western blot analysis was used to analyze the expression of epidermal growth factor receptor (EGFR) and its downstream signaling pathway extracellular signal-regulated kinase (ERK) protein in H2O2. Results show that after applying low concentration of H2O2 treatment on AGS cells for 48 hours, EGFR protein levels and ERK protein phosphorylation levels increased significantly. These results suggest that low concentration of H2O2 can significantly increase the proliferation of AGS cells by EGFR/ERK signaling pathway. [ LINK ]

In the following study, researchers examine visfatin expression and its effect on telomerase gene expression in AGS cells. Reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosobent assay were performed to analyze visfatin expression in mRNA and protein level. Total RNA was extracted and complementary deoxyribonucleic acid was synthesized to analyze telomerase gene expression. Results show that visfatin induces AGS cell proliferation and increases telomerase (hTERT) gene expression, which suggest that expression of visfatin in real protein in real samples could be a biomarker for gastric cancer. [ LINK ]

In the following study, researchers investigated the effects of BP-1-102, a novel inhibitor of signal transducer and activator of transcription 3 (STAT3), on AGS cells. Flow cytometric analysis and Western blot analysis revealed that BP-1-102 induces apoptosis and inhibited the phosphorylation of STAT3 and its target genes in a time- and dose-dependent manner. These results indicate that BP-1-102 has the potential to be used as an antitumor agent in AGS cells through the modulation of STAT3 signaling pathways. [ LINK ]