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Epha3 acts as proangiogenic factor in multiple myeloma
Antonella Caivano1, Francesco La Rocca1, Ilaria Laurenzana1
1Laboratory of Pre-clinical and Translational Research, Scientific Institute of Research and Cure (IRCCS), Referral Cancer Center of Basilicata (CROB), Rionero in Vulture, Italy.
Oncotarget
|April 19, 2017
Summary
Ephrin receptor A3 (EphA3) is highly expressed in multiple myeloma (MM) and drives angiogenesis. Targeting EphA3 with an antibody or siRNA inhibits MM endothelial cell functions, suggesting EphA3 as a therapeutic target for MM angiogenesis.
Area of Science:
- Oncology
- Cell Biology
- Molecular Medicine
Background:
- Angiogenesis is crucial for multiple myeloma (MM) progression.
- The role of specific molecular targets in MM-associated angiogenesis requires further elucidation.
Purpose of the Study:
- To investigate the role of ephrin receptor A3 (EphA3) in the angiogenesis of MM.
- To evaluate the effects of targeting EphA3 on primary bone marrow endothelial cells (ECs) from MM patients.
Main Methods:
- Quantitative analysis of EphA3 mRNA and protein in MM patient-derived ECs (MMECs), monoclonal gammopathy ECs (MGECs), and control ECs.
- In vitro functional assays including cell adhesion, migration, and tube formation.
- Evaluation of EphA3 targeting via siRNA-mediated knockdown and a specific anti-EphA3 monoclonal antibody.
- Gene expression profiling following EphA3 knockdown.
Main Results:
- EphA3 demonstrated significantly higher expression in MMECs compared to MGECs and control ECs.
- EphA3 knockdown using siRNA impaired MMEC adhesion, migration, and tube formation in vitro, without affecting proliferation or viability.
- Gene expression analysis revealed that EphA3 knockdown modulated genes involved in adhesion, migration, and invasion.
- Treatment with an anti-EphA3 antibody recapitulated the inhibitory effects on MMEC angiogenesis-related functions.
Conclusions:
- Ephrin receptor A3 (EphA3) plays a critical role in promoting multiple myeloma (MM) angiogenesis.
- Targeting EphA3 represents a potential therapeutic strategy to inhibit MM angiogenesis.