Rabbit Anti-Human EFNA3 (a.a. 101-200) Polyclonal antibody

Eph receptors and ephrin ligands are master regulators of oncogenic signaling required for proliferation, migration, and metastasis. Yet, Eph/ephrin expression and activity in medulloblastoma (MB), the most common malignant brain tumor of childhood, remains poorly defined. We hypothesized that Eph/ephrins are differentially expressed by sonic hedgehog (SHH) and non-SHH MB and that specific members contribute to the aggressive phenotype. Affymetrix gene expression profiling of 29 childhood MB, separated into SHH (N = 11) and non-SHH (N = 18), was performed followed by protein validation of selected Eph/ephrins in another 60 MB and two MB cell lines (DAOY, D556). Functional assays were performed using MB cells overexpressing or deleted for selected ephrins. We found EPHB4 and EFNA4 almost exclusively expressed by SHH MB, whereas EPHA2, EPHA8, EFNA1 and EFNA3 are predominantly expressed by non-SHH MB. The remaining family members, except EFNB1, are ubiquitously expressed by over 70-90 % MB, irrespective of subgroup. EFNB1 is the only member differentially expressed by 28 % of SHH and non-SHH MB. Corresponding protein expression for EphB/ephrinB1 and B2 was validated in MB. Only ephrinB2 was also detected in fetal cerebellum, indicating that EphB/ephrinB1 expression is MB-specific. EphrinB1 immunopositivity localizes to tumor cells within MB with the highest proliferative index. EphrinB1 overexpression promotes EphB activation, alters F-actin distribution and morphology, decreases adhesion, and significantly promotes proliferation. Either silencing or overexpression of ephrinB1 impairs migration. These results indicate that EphrinB1 is uniquely dysregulated in MB and promotes oncogenic responses in MB cells, implicating ephrinB1 as a potential target.

Background:Gastric cancer (GC) is one of the most common malignancies worldwide, exhibiting a high morbidity, and mortality. As the various treatment methods for gastric cancer are limited by disadvantages, many efforts to improve the efficacy of these treatments are being taken. Metabolic recombination is an important characteristic of cancer and has gradually caused a recent upsurge in research. However, systematic analysis of the interaction between glycolysis and GC patient prognosis and its potential associations with immune infiltration is lacking but urgently needed. Methods:We obtained the gene expression data and clinical materials of GC derived from The Cancer Genome Atlas (TCGA) dataset. Univariate and multivariate Cox proportional regression analyses were performed to select the optimal prognosis-related genes for subsequent modeling. We then validated our data in the GEO database and further verified the gene expression using the Oncomine database and PCR experiments. Besides, Gene set variation analysis (GSVA) analysis was employed to further explore the differences in activation status of biological pathways between the high and low risk groups. Furthermore, a nomogram was adopted to predict the individualized survival rate of GC patients. Finally, a violin plot and a TIMMER analysis were performed to analyse the characteristics of immune infiltration in the microenvironment. Results:A seven-gene signature, including STC1, CLDN9, EFNA3, ZBTB7A, NT5E, NUP50, and CXCR4, was established. Based on this seven-gene signature, the patients in the training set and testing sets could be divided into high-risk and low-risk groups. In addition, a nomogram based on risk and age showed good calibration and moderate discrimination. The results proved that the seven-gene signature had a strong capacity to predict the GC patient prognosis. Collectively, the violin plot and TIMMER analysis demonstrated that an immunosuppressive tumor microenvironment caused by hyperglycolysis led to poor prognosis. Conclusion:Taken together, these results established a genetic signature for gastric cancer based on glycolysis, which has reference significance for the in-depth study of the metabolic mechanism of gastric cancer and the exploration of new clinical treatment strategies.