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Updated: Jun 23, 2026

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Published on: January 10, 2025
Overexpression of Midkine promotes the viability of BA/F3 cells
Yang Wang1, Haiyan Xing, Zheng Tian
1State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Disease Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin 300020, PR China.
Abstract:
Midkine (MK), a heparin-binding growth factor, has been reported to be overexpressed in a variety of human solid tumors. In the previous study, we found that MK was overexpressed in bone marrow samples derived from acute leukemia (AL) patients. To elucidate the role of MK, we stably transfected MK in IL-3-dependent BA/F3 cells. The results indicated that the capacity of proliferation and colony formation was significantly increased in the MK-transfected subclones than in the empty vector-transfected subclones. MK potentiated proliferation of BA/F3 cells by promoting cell cycle progression. Apoptosis assays showed a remarkable reduction of apoptosis in MK expressing subclones. Exogenous MK could induce the phosphorylation of Raf-1, and inhibit the expression of Bax in BA/F3 cells. These results indicate that MK might be involved in the pathogenesis of leukemia and could be taken as an ideal diagnostic marker and molecular target for the treatment of acute leukemia.
Insights
Midkine (MK) promotes acute leukemia cell growth and survival. This growth factor enhances proliferation and colony formation while reducing apoptosis, suggesting its role in leukemia pathogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Hematology
Background:
- Midkine (MK), a heparin-binding growth factor, is overexpressed in various human solid tumors.
- Previous research identified MK overexpression in bone marrow of acute leukemia (AL) patients.
Purpose of the Study:
- To investigate the functional role of Midkine (MK) in acute leukemia.
- To elucidate the mechanisms by which MK influences leukemia cell behavior.
Main Methods:
- Stable transfection of Midkine (MK) into IL-3-dependent BA/F3 cells.
- Assays for proliferation, colony formation, cell cycle progression, and apoptosis.
- Western blot analysis to assess Raf-1 phosphorylation and Bax expression.
Main Results:
- MK-transfected cells showed significantly increased proliferation and colony formation compared to controls.
- MK expression enhanced cell cycle progression and markedly reduced apoptosis.
- Exogenous MK induced Raf-1 phosphorylation and inhibited Bax expression.
Conclusions:
- Midkine (MK) plays a significant role in the pathogenesis of acute leukemia.
- MK promotes leukemia cell proliferation and survival, suggesting its potential as a diagnostic marker and therapeutic target for AL.

