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Hepatocyte Growth Factor: A Microenvironmental Resource for Leukemic Cell Growth
Paolo Giannoni1, Franco Fais2, Giovanna Cutrona3
1Stem Cell Laboratory, Department of Experimental Medicine, University of Genoa, V. Pastore 3, 16132 Genova, Italy. paolo.giannoni@unige.it.
International Journal of Molecular Sciences
|January 16, 2019
Summary
Hepatocyte growth factor (HGF) produced by the microenvironment sustains chronic lymphocytic leukemia (CLL) cell survival and promotes immune suppression. Blocking HGF/c-MET interactions may offer novel therapeutic strategies for CLL.
Area of Science:
- Hematology
- Cancer Biology
- Immunology
Background:
- Chronic lymphocytic leukemia (CLL) involves the accumulation of malignant B lymphocytes (CD5+/CD23+).
- The tumor microenvironment plays a critical role in CLL pathogenesis and progression.
- Nurse-like cells (NLCs) within the CLL microenvironment support leukemic cell survival.
Purpose of the Study:
- To investigate the role of hepatocyte growth factor (HGF) and its receptor c-MET in CLL.
- To elucidate the mechanisms by which the microenvironment influences CLL cell survival and immune response.
- To explore novel therapeutic strategies targeting the HGF/c-MET pathway.
Main Methods:
- Analysis of HGF and c-MET expression in CLL cells and microenvironment.
- Assessment of signaling pathways (STAT3, AKT) activated by HGF/c-MET interaction.
- Investigation of HGF's effect on monocyte differentiation towards M2 phenotype.
Main Results:
- Bone marrow stromal and trabecular bone cells produce HGF, sustaining CLL cell survival.
- HGF/c-MET signaling activates STAT3 and AKT pathways in CLL cells.
- HGF induces monocyte differentiation into M2-like macrophages, contributing to immune suppression.
Conclusions:
- HGF produced by the microenvironment and potentially by CLL cells promotes leukemic cell survival and immune evasion.
- The HGF/c-MET axis represents a potential therapeutic target for CLL and other hematological malignancies.
- Blocking HGF/c-MET interactions could overcome drug resistance and improve treatment outcomes in CLL.
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