Jagged Ligands Enhance the Pro-Angiogenic Activity of Multiple Myeloma Cells.
Maria Teresa PalanoDomenica GiannandreaNatalia PlatonovaGermano GaudenziMonica FalleniDelfina TosiElena LesmaValentina CitroMichela ColomboIlaria SaltarellaRoberto RiaNicola AmodioElisa TaianaAntonino NeriGiovanni VitaleRaffaella ChiaramontePublished in: Cancers (2020)
Multiple myeloma (MM) is an incurable plasma cell malignancy arising primarily within the bone marrow (BM). During MM progression, different modifications occur in the tumor cells and BM microenvironment, including the angiogenic shift characterized by the increased capability of endothelial cells to organize a network, migrate and express angiogenic factors, including vascular endothelial growth factor (VEGF). Here, we studied the functional outcome of the dysregulation of Notch ligands, Jagged1 and Jagged2, occurring during disease progression, on the angiogenic potential of MM cells and BM stromal cells (BMSCs). Jagged1-2 expression was modulated by RNA interference or soluble peptide administration, and the effects on the MM cell lines' ability to induce human pulmonary artery cells (HPAECs) angiogenesis or to indirectly increase the BMSC angiogenic potential was analyzed in vitro; in vivo validation was performed on a zebrafish model and MM patients' BM biopsies. Overall, our results indicate that the MM-derived Jagged ligands (1) increase the tumor cell angiogenic potential by directly triggering Notch activation in the HPAECs or stimulating the release of angiogenic factors, i.e., VEGF; and (2) stimulate the BMSCs to promote angiogenesis through VEGF secretion. The observed pro-angiogenic effect of Notch activation in the BM during MM progression provides further evidence of the potential of a therapy targeting the Jagged ligands.
Keyphrases
- endothelial cells
- vascular endothelial growth factor
- induced apoptosis
- pulmonary artery
- multiple myeloma
- cell cycle arrest
- bone marrow
- high glucose
- coronary artery
- pulmonary hypertension
- cell proliferation
- poor prognosis
- single cell
- human health
- ejection fraction
- oxidative stress
- newly diagnosed
- end stage renal disease
- mesenchymal stem cells
- risk assessment
- chronic kidney disease
- binding protein
- cell death
- climate change