The EphB4 Receptor Promotes The Growth Of Melanoma Cells Expressing The Ephrin‐B2 Ligand

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NIH Public Access 1,2,† 2,‡ James S. Goydos3 Dana Yip3 Ameae

The EphB4 receptor promotes the growth of melanoma cells expressing the ephrin-B2 ligand Nai-Ying Yang1,2,†, Pablo Lopez-Bergami2,‡, James S. Goydos3, Dana Yip3, Ameae M. Walker1, Elena B. Pasquale2,4, and Iryna Ethell1,† 1Division of Biomedical Sciences, University of California Riverside, Riverside, CA, USA

Development of non-viral, ligand-dependent, EPHB4-specific

EPHRIN B2-mediated EPHB4 activation by EPHB4-CAR-T cells did not induce RMS cell proliferation Because the antigen-recognition site of EPHB4-CAR utilizes the nat-ural ligand of EPHB4 (EPHRIN B2), EPHB4-CAR-T cells not only bind to EPHB4 but also stimulate it, leading to downstream activa-tion of EPHB4 via ligand-receptor interaction.

TheEphB4Receptor-tyrosineKinasePromotestheMigration

melanoma cells with well defined metastatic properties in vivo and migratory abilities in vitro, we show that the EphB recep-tors enhance the migration of melanoma cells. Highly malig-nant melanoma cells that migrate rapidly express the highest levels of EphB receptors, including EphB2, EphB3, and EphB4.

Research EphB4 Promotes Site-Specific Metastatic Tumor Cell

adhesion of EphB4-expressing tumor cells to ephrinB2-expressing endothelial cells. Screening of a panel of human tumor cell lines identified EphB4 expression in nearly all analyzed tumor cell lines. Human A375 mel-anoma cells engineered to express either full-length EphB4 or truncated EphB4 variants which lack the cytoplas-

Supplementary Information

Supplementary Fig. S2. Roquin2 inhibits tumor cells-induced angiogenesis. (A, B) Cell lystates from MDA-MB-231 (A) and MCF7 (B) cells expressing Roquin2-GFP fusion protein or GFP were harvested for immunobloting analysis with anti-GFP and anti-β-actin antibodies. (C)

ParadoxesoftheEphB4ReceptorinCancer

ligand ephrin-B2 also has the ability to generate signals through its cytoplasmic domain, which are known as reverse signals (1). These signals can be stimulated by endogenous EphB4 or by EphB4 Fc (1, 11) and may contribute to maintain an epithelial phenotype (12), but their identity in epithelial cells is unknown (Fig. 1B).

PEGylation Potentiates the Effectiveness of an Antagonistic

tumor progression is to promote ephrin-B2 reverse signaling in the vasculature. This role may be fulfilled by EphB4 present in tumor cells or co-expressed in vascular cells [13,14,15,22]. Additionally, ephrin-B2-induced EphB4 forward signaling in endothelial cells likely contributes to tumor angiogenesis [13,14,16,19,23,24].