ArticleBlood advances2020
The EGFL7-ITGB3-KLF2 axis enhances survival of multiple myeloma in preclinical models.
Article in Blood advances, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
- Multiple myeloma: A tale of deregulated transcription factors.HemaSphere · 2026Review
- EGFL7 Inhibits the Immune Response in Metastatic Castration-Resistant Prostate Cancer by Deactivating Endothelial Intercellular Adhesion Molecule-1.The world journal of men's health · 2026Article
- Integrated RNA-seq and RT-qPCR Workflow Identifies Non-IGH Fusion Transcripts as Individualized Molecular Markers for Monitoring Multiple Myeloma.Biomedicines · 2026Article
- Enhancing radiosensitivity of osteosarcoma by ITGB3 knockdown: a mechanism linked to enhanced osteogenic differentiation status through JNK/c-JUN/RUNX2 pathway activation.Journal of experimental & clinical cancer research : CR · 2025Article
- Pan-cancer analysis of ITGB3 as a potential prognostic and immunological biomarker.Discover oncology · 2025Article
- A novel mechanism in regulating drug sensitivity, growth, and apoptosis of bortezomib-resistant multiple myeloma cells: the USP4/KLF2/HMGA2 cascade.Journal of orthopaedic surgery and research · 2025Article
- Identification of the EBF1/ETS2/KLF2-miR-126-Gene Feed-Forward Loop in Breast Carcinogenesis and Stemness.International journal of molecular sciences · 2025Article
- Mesenchymal stem cells reverse thymus aging by reprogramming the DNA methylation of thymic epithelial cells.Regenerative therapy · 2024Article
- Heparin-binding EGF-like growth factor via miR-126 controls tumor formation/growth and the proteolytic niche in murine models of colorectal and colitis-associated cancers.Cell death & disease · 2024Article
- Progression of monoclonal gammopathy of undetermined significance to multiple myeloma is associated with enhanced translational quality control and overall loss of surface antigens.Journal of translational medicine · 2024Article
- The influence of 4G/5G polymorphism in the plasminogen-activator-inhibitor-1 promoter on COVID-19 severity and endothelial dysfunction.Frontiers in immunology · 2024Article
- PRC2 mediated KLF2 down regulation: a therapeutic and diagnostic axis during tumor progression.Cancer cell international · 2023Review
- Krüppel-like factor 2: a central regulator of B cell differentiation and plasma cell homing.Frontiers in immunology · 2023Review
- Relation among EGFL7, ITGB3, and KLF2 and their clinical implication in multiple myeloma patients: a prospective study.Irish journal of medical science · 2022Article
- ERK5 Is a Major Determinant of Chemical Sarcomagenesis: Implications in Human Pathology.Cancers · 2022Article
- Review
- Review
- Cancer-Associated Angiogenesis: The Endothelial Cell as a Checkpoint for Immunological Patrolling.Cancers · 2020Review
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiogenic factors play a key role in multiple myeloma (MM) growth, relapse, and drug resistance. Here we show that malignant plasma cells (cell lines and patient-derived MM cells) express angiocrine factor EGF like-7 (EGFL7) mRNA and protein. MM cells both produced EGFL7 and expressed the functional EGFL7 receptor integrin β 3 (ITGB3), resulting in ITGB3 phosphorylation and focal adhesion kinase activation. Overexpression of ITGB3 or EGFL7 enhanced MM cell adhesion and proliferation. Intriguingly, ITGB3 overexpression upregulated the transcription factor Krüppel-like factor 2 (KLF2), which further enhanced EGFL7 transcription in MM cells, thereby establishing an EGFL7-ITGB3-KLF2-EGFL7 amplification loop that supports MM cell survival and proliferation. EGFL7 expression was found in certain plasma cells of patients with refractory MM and of patients at primary diagnosis. NOD.CB17-Prkdc<scid>/J mice transplanted with MM cells showed elevated human plasma EGFL7 levels. EGFL7 knockdown in patient-derived MM cells and treatment with neutralizing antibodies against EGFL7 inhibited MM cell growth in vitro and in vivo. We demonstrate that the standard-of-care MM drug bortezomib upregulates EGFL7, ITGB3, and KLF2 expression in MM cells. Inhibition of EGFL7 signaling in synergy with BTZ may provide a novel strategy for inhibiting MM cell proliferation.
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