Glycoprotein nonmetastatic melanoma protein B impacts the malignant potential of bladder cancer cells through its hem-immunoreceptor tyrosine-based activation motif.

Bladder cancer is one of the most common cancers among men worldwide. Although multiple genomic mutations and epigenetic alterations have been identified, an efficacious molecularly targeted therapy has yet to be established. Therefore, a novel approach is anticipated.

Glycoprotein non-metastatic melanoma protein B functions with growth factor signaling to induce tumorigenesis through its serine phosphorylation.

Breast cancer is the most common cancer among women. Glycoprotein non-metastatic melanoma protein B (GPNMB), a type I transmembrane protein that is highly expressed in many cancers, including breast cancer, has been shown to be a prognostic factor. We previously reported that GPNMB overexpression confers tumorigenic potential, as evidenced by invasive tumor growth in vivo, sphere formation, and cellular migration and invasion to non-tumorigenic mammary epithelial cells.

Messenger RNA translation enhancement by immune evasion proteins: a comparative study between EKB (vaccinia virus) and NS1 (influenza A virus).

In this study, we compared vaccinia virus derived monofunctional E3, K3 and B18R (also known as EKB) with influenza A virus derived multifunctional non-structural protein 1 (NS1) based on their ability to enhance mRNA translation. EKB and NS1-TX91 were all found to enhance mRNA translation and suppress interferon production, yet level of enhancement by EKB was much lower than NS1-TX91. Similarly, greater luciferase expression was mediated by co-delivery of unmodified luciferase with NS1 mRNA, compared to co-delivery of unmodified luciferase with either E3, K3 or B18R mRNA, respectively.