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Updated: Apr 12, 2026
Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line
Published on: August 2, 2021
[Macrophage inflammatory protein-1α promotes the growth of acute myeloid leukemia cells]
Ping Lu1, Ya-Jie Wang1, Ya-Wei Zheng1
1State Key Laboratory of Experimental Hematology, Institute of Hematology & Blood Disease Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300020, China.
Unlabelled:
BACKGROWND: Macrophage inflammatory protein-1α (MIP-l α/CCL3) belongs to the C-C chemokine family (CCL3), which can be secreted by macrophages, other types of hematopoietic cells and bone marrow stromal cells. Higher levels of MIP-1α were found to be associated with several kinds of hematologic malignancies, including multiple myeloma (MM), chronic lymphocytic leukemia (CLL) and chronic myeloid leukemia (CML). Moreover, MIP-1α has been reported to be an adverse prognostic factor for CLL. However, the impact of MIP-1α on acute myeloid leukemia (AML) has been poorly investigated.
Objective:
To investigate the influence of MIP-1α on proliferction of AML cells.
Methods:
Using MLL-AF9 induced AML mouse model, the expression of MIP-1α was measured by real time quantitative RT-PCR. AML cell proliferation was examined by cell counting and colony forming assay (CFC). The influence of blocking the MIP-1α action on the growth and pathogenic ability of AML cells was explored by using the small molecule antagonist for interfering interaction of MIP-1α with its receptor CCR1.
Results:
The MIP-1α could promote the proliferation and colony formation of AML cells, the blocking MIP-1a could inhibit the growth of AML cells and delay onset of AML.
Conclusion:
The MIP-1a promotes the occurence and progression of AML, therefore blocking the MIP-1α signal pathway may be served as a strategy to inhibit the growth of AML cells, and MIP-1α can be a potential target for treatment of AML.
Insights
Macrophage inflammatory protein-1α (MIP-1α) promotes acute myeloid leukemia (AML) cell growth and progression. Blocking MIP-1α signaling may inhibit AML cell proliferation and serve as a potential therapeutic strategy.
Area of Science:
- Hematology
- Immunology
- Oncology
Context:
- Macrophage inflammatory protein-1α (MIP-1α/CCL3) is a C-C chemokine implicated in various hematologic malignancies.
- Elevated MIP-1α levels are associated with multiple myeloma, chronic lymphocytic leukemia (CLL), and chronic myeloid leukemia (CML).
- MIP-1α is a known adverse prognostic factor in CLL, but its role in acute myeloid leukemia (AML) is understudied.
Purpose:
- To investigate the influence of MIP-1α on the proliferation of acute myeloid leukemia (AML) cells.
- To explore the therapeutic potential of blocking MIP-1α signaling in AML.
Summary:
- A MLL-AF9 induced AML mouse model was utilized to assess MIP-1α expression via RT-PCR.
- AML cell proliferation was evaluated using cell counting and colony-forming assays (CFC).
- The effect of a small molecule antagonist targeting the MIP-1α/CCR1 interaction was examined to inhibit AML cell growth and pathogenic ability.
Impact:
- MIP-1α significantly promotes AML cell proliferation and colony formation.
- Blocking MIP-1α action inhibited AML cell growth and delayed disease onset in the mouse model.
- These findings suggest that MIP-1α is a potential therapeutic target for AML treatment, with blocking its pathway offering a viable strategy to inhibit cancer cell growth.
