Abstract
The erythropoietin-producing hepatocellular carcinoma (Eph) receptors and their Eph receptor-interacting (ephrin) ligands together constitute a vital cell communication system with diverse roles. Experimental evidence revealed Eph receptor bidirectional signaling with both tumor-promoting and tumor-suppressing activities in different cancer types and surrounding environment. Eph receptor B2 (EphB2), an important member of the Eph receptor family, has been proved to be aberrantly expressed in many cancer types, such as colorectal cancer, gastric cancer and hepatocellular carcinoma, resulting in tumor occurrence and progression. However, there are no reviews focusing on the dual roles of EphB2 in cancer. Thus, in this paper we systematically summarize and discuss the roles of EphB2 in cancer. Firstly, we review the main biological features and the related signaling regulatory mechanisms of EphB2, and then we summarize the roles of EphB2 in cancer through current studies. Finally, we put forward our viewpoint on the future prospects of cancer research focusing on EphB2, especially with regard to the effects of EphB2 on tumor immunity.
Highlights
The erythropoietin-producing hepatocellular carcinoma (Eph) receptors constitute the largest subfamily of receptor tyrosine kinases (RTKs) identified until now (Eph Nomenclature Committee, 1997)
Eph receptor B2 (EphB2) is a significant member of the Eph receptor family, which was thought to be distributed on tumor cells and endothelial cells in previous researches (Salvucci et al, 2006; Wang et al, 2012)
As EphB2 was found to be expressed on some immunocytes such as monocytes, T cells, and B cells, increasing researches have reported on the roles of EphB2 in immunity (Alfaro et al, 2008; Braun et al, 2011; Yu et al, 2014)
Summary
The erythropoietin-producing hepatocellular carcinoma (Eph) receptors constitute the largest subfamily of receptor tyrosine kinases (RTKs) identified until now (Eph Nomenclature Committee, 1997). Eph receptors interact with their membrane-bound ligands the ephrins and promote cell-cell contacts, leading to bidirectional intracellular signaling and downstream signaling cascades that induce autophosphorylation of tyrosine residues in the juxtamembrane region and kinase domain, which further drive the recruitment of downstream signaling molecules (Kullander and Klein, 2002). These include Src family kinases, mitogen-activated protein (MAP) kinases, Src homology 2 and 3 adapter proteins, guanine nucleotide exchange factors, phosphatidylinositol 3-kinase (PI3K), small GTPases, and phosphatases. Mutational inactivation of EPHB2 may play an important role in cancer progression (Huusko et al, 2004)
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