Anti-EFEMP1 monoclonal antibody, clone 2E0

Objective: We aimed to investigate the effect of miR-338-5p on proliferation, migration and invasion of glioblastoma (GBM) cells by regulating EFEMP1. Methods: The expression of miR-338-5p and EFEMP1 was measured by qRT-PCR and western blot. Transfection was conducted to regulate the expression of miR-338-5p and EFEMP1 in U87 cell lines. Cell proliferation, apoptosis, migration and invasion were evaluated using CCK-8 assay, flow cytometry and Transwell assay respectively. Dual luciferase reporter assay was performed to verify whether miR-338-5p directly targeted EFEMP1. Results: MiR-338-5p was significantly down-regulated in human GBM tumor tissues and cells while EFEMP1 was strongly upregulated (P < 0.05). Upregulated miR-338-5p was able to suppress cell proliferation, migration, invasion, and promote cell apoptosis in GBM cells (P < 0.05). Dual luciferase reporter gene assay determined that miR-338-5p directly targeted EFEMP1 (P < 0.05). Conclusions: MiR-338-5p suppressed proliferation, migration and invasion of GBM cells through inhibiting EFEMP1. (c) 2017 Published by Elsevier Masson SAS.

Carpal tunnel syndrome (CTS) is a common and disabling condition of the hand caused by entrapment of the median nerve at the level of the wrist. It is the commonest entrapment neuropathy, with estimates of prevalence ranging between 5-10%. Here, we undertake a genome-wide association study (GWAS) of an entrapment neuropathy, using 12,312 CTS cases and 389,344 controls identified in UK Biobank. We discover 16 susceptibility loci for CTS with p < 5 x 10(-8). We identify likely causal genes in the pathogenesis of CTS, including ADAMTS17, ADAMTS10 and EFEMP1, and using RNA sequencing demonstrate expression of these genes in surgically resected tenosynovium from CTS patients. We perform Mendelian randomisation and demonstrate a causal relationship between short stature and higher risk of CTS. We suggest that variants within genes implicated in growth and extracellular matrix architecture contribute to the genetic predisposition to CTS by altering the environment through which the median nerve transits.