Anti-GKN1 (full length) polyclonal antibody

Trefoil factor 1 (TFF1) is a small cysteine-rich secreted protein which is principally expressed in the superficial cells of gastric mucosa. In gastric cancer, TFF1 is downregulated and plays an important role. Gastrokine 1 (GKN1) is a secreted protein with similar expression and biological functions to TFF1. This study aimed to determine the expression and biological functions of TFF1 and the relationships between TFF1 and GKN1 in gastric cancer. RT-PCR and immunohistochemistry were performed to detect TFF1 expression in gastric cancer cell lines and tissues. The transfected and co-transfected AGS cells which stably expressed TFF1 or both TFF1 and GKN1 were generated. Phenotypic changes such as cell viability, apoptosis and cell cycle modulation were assayed in the transfected cells. We found that TFF1 expression was significantly downregulated or lost in gastric cancer cell lines, gastric dysplasia and cancer. Restoration of TFF1 expression in AGS cells suppressed tumor cell viability and arrested AGS cells in the G1-S transition phase after olomoucine treatment. However, TFF1 was unable to induce cell apoptosis. In co-transfected cells, we found that TFF1 and GKN1 did not directly interact at the protein level. GKN1 was unable to cooperate with TFF1 on cell viability suppression, cell apoptosis and differentiation. Together, these results indicate that TFF1 expression is significantly downregulated in gastric cancer. TFF1 inhibited cell proliferation by delaying G1-S phase transition but not by inducing apoptosis. TFF1 may not interact or cooperate with GKN1 at the protein and functional level.

Gastrokines (GKNs) are bioactive substances secreted by gastric cells. Evidence supports functional roles for GIC\is in gastric homeostasis, immune responses and tumour suppression. Down-regulation has been reported in Helicobacter pylori associated gastritis and other inflammatory gastrointestinal conditions in mice and people. The aim of this study was to evaluate GKN gene expression in dogs positive for other Helicobacter spp. both before and after treatment. Expression of Gkn-1 and Gkn-2 mRNA was studied in endoscopic biopsy samples collected from seven healthy dogs over three time-points pre- (TO) and at 1 and 18 weeks post-treatment for Helicobacter spp. colonisation (T1 & T2). The relative expression software tool (REST) was used to provide efficiency corrected expression ratios for comparisons between groups and these results were compared to a standard 2 Delta Delta CT methodology. Compared with T1 Gknl and Gkn2 mRNA expression was greater at TO by a mean factor of 2.53 (SE = 1.83-3.54) for Gknl (P = 0.000) and 2.85 (SE = 2.23-3.75) for Gkn2 (P = 0.000). This difference was attenuated when comparisons were made between TO and T2. Histopathological evidence of gastritis was not present in any Helicobacter spp. positive sample. When compared to post-eradication samples Gkn gene expression is increased in the presence of Helicobacter spp. in dogs without evidence for concurrent inflammation. Further evaluation is required to determine the relevance of this finding, however given a suspected role in gastric homeostasis, up-regulation of GKN1 and GKN2 could limit development of gastritis in Helicobacter spp. positive dogs.