Rabbit anti-GSPT1 Polyclonal antibody

Gastric cancer remains a major cause of death in the developed countries, and a large percentage is still genetically unexplained. Because of their major role in cell survival, mutations in translation factors and altered expression of these genes have been associated with cancer development. Apart from its role in translation termination, the eukaryotic translation release factor 3 (eRF3) is involved in several critical cellular processes, such as cell cycle regulation, cytoskeleton organization and apoptosis. The aim of this study was to evaluate eRF3/GSPT1 gene as a potential genetic susceptibility associated locus for gastric cancer, analysing a stable GGC expansion in exon 1 encoding a polyglycine tract in the N-terminal domain of the protein. DNA was obtained from 139 patients with gastric cancer and from 100 individuals of a healthy control population. The GGC expansion was amplified by PCR and the number of repeats determined by genotyping in an automatic sequencer. There are five known alleles encoding from 8 to 12 glycines. The most common allele encodes 10 glycines. The 12-Gly allele was detected exclusively in the cancer patients (allelic frequency = 5%). Regardless of the genotype, patients with the 12-Gly allele had a 20-fold increased risk for gastric cancer. We also detected a single-base alteration in the gene (G274T) although no correlation with cancer development has been found. Thus, our results show that the GGC expansion may have a potential role in regulating eRF3/GSPT1 expression and/or changing the protein function that can lead to gastric cancer development.

OBJECTIVE: To investigate the potential effects of miR-144/GSPT1 axis on the development of gastric cancer. PATIENTS AND METHODS: The expressions of GSPT1 (G1 to S Phase Transition 1) and miR-144 were detected in gastric cancer tissues and the adjacent normal tissues. We also explored the levels of GSPT1 and miR-144 in both normal gastric cell line (GES-1) and gastric cells (SGC7901). Luciferase assay was conducted to evaluate the interaction between miR-144 and GSPT1. The effects of the miR-144/GSPT1 axis on SGC7901 cells were determined via investigating cell proliferation, invasion and metastasis. RESULTS: miR-144 was found to be down-regulated in gastric cancer tissues while GSPT1 expression level was markedly increased. Bioinformatics analysis showed that GSPT1 was a direct target of miR-144. Luciferase assays confirmed our hypothesis. The subsequent experiments showed that miR-144 could promote cell proliferation, invasion and migration in gastric cancer cells via inhibiting GSPT1. CONCLUSIONS: We showed that miR-144/GSPT1 axis could be a potential therapeutic target in treatment of gastric cancer.