NDLI: EphA3 targeting reduces in vitro adhesion and invasion and in vivo growth and angiogenesis of multiple myeloma cells

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Cellular Oncology : Volume 40, Issue 4, August 2017

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Cellular Oncology : Volume 40, Issue 1, February 2017

Cellular Oncology : Volume 39

Cellular Oncology : Volume 38

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Cellular Oncology : Volume 36

Cellular Oncology : Volume 35

Cellular Oncology : Volume 34

EphA3 targeting reduces in vitro adhesion and invasion and in vivo growth and angiogenesis of multiple myeloma cells

Content Provider	Springer Nature Link
Author	Rocca, Francesco Airoldi, Irma Carlo, Emma Marotta, Pina Falco, Geppino Simeon, Vittorio Laurenzana, Ilaria Trino, Stefania Luca, Luciana Todoerti, Katia Villani, Oreste Lackmann, Martin D’Auria, Fiorella Frassoni, Francesco Neri, Antonino Vecchio, Luigi Musto, Pellegrino Cilloni, Daniela Caivano, Antonella
Copyright Year	2017
Abstract	Multiple myeloma (MM) is a hematologic malignancy characterized by a clonal expansion of plasma cells (PCs) in the bone marrow (BM). Since MM has so far remained incurable, further insights into its pathogenesis and the concomitant identification of new therapeutic targets are urgently needed. The tyrosine kinase receptor EphA3 is known to be involved in various cellular processes including cell viability, cell movement and cell-cell interactions. Recently, EphA3 has emerged as a potential therapeutic target in several hematologic and solid tumors. Here, we aimed to uncover the role of EphA3 in MM.EphA3 mRNA and protein expression in primary MM bone marrow plasma cells (BMPCs), in MM-derived cell lines and in healthy controls (HCs) was assessed using qRT-PCR, Western blotting and flow cytometry. The effects of siRNA-mediated EphA3 silencing and anti EphA3 antibody (EphA3mAb) treatment on MM PC trafficking and viability were evaluated using in vitro assays. The effects of EphA3mAb treatment were also assessed in two MM-derived mouse xenograft models.We found that EphA3 was overexpressed in primary MM BMPCs and MM-derived cell lines compared to HCs. We also found that siRNA-mediated EphA3 silencing and EphA3mAb treatment significantly inhibited the ability of MM PCs to adhere to fibronectin and stromal cells and to invade in vitro, without affecting cell proliferation and viability. Gene expression profiling showed that EphA3 silencing resulted in expression modulation of several molecules that regulate adhesion, migration and invasion processes. Importantly, we found that EphA3mAb treatment significantly inhibited in vivo tumor growth and angiogenesis in two MM-derived mouse xenograft models.Our findings suggest that EphA3 plays an important role in the pathogenesis of MM and provide support for the notion that its targeting may represent a novel therapeutic opportunity for MM.
Starting Page	483
Ending Page	496
Page Count	14
File Format	PDF
ISSN	22113428
Journal	Cellular Oncology
Volume Number	40
Issue Number	5
e-ISSN	22113436
Language	English
Publisher	Springer Netherlands
Publisher Date	2017-07-18
Publisher Institution	International Society for Cellular Oncology
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Multiple myeloma Plasma cells EphA3 Cell movement Anti EphA3 monoclonal antibody Cancer Research Biomedicine Pathology Oncology
Content Type	Text
Resource Type	Article
Subject	Cancer Research Molecular Medicine Oncology

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