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Updated: May 8, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Fibrinogen promotes acute myelogenous leukemia progression via miR-486/GPR153 axis
Ming Yang1, Xiaofang You2, Fan Zhao3
1State Key Laboratory of Genetics and Development of Complex Phenotypes, School of Life Sciences, Zhongshan Hospital, Fudan University, Shanghai 200438, China; Shanghai Key Laboratory of Gene Editing and Cell Therapy for Rare Diseases, Engineering Research Center of Gene Technology (Ministry of Education), Fudan University, Shanghai 200031.
Fibrinogen accelerates acute myeloid leukemia (AML) progression by upregulating miR-486-5p, targeting GPR153 and activating the mTORC2/AKT pathway. This discovery offers new therapeutic targets for AML treatment.
Area of Science:
- Hematology
- Molecular Biology
- Oncology
Background:
- Acute myeloid leukemia (AML) is a fatal bone marrow malignancy.
- Fibrinogen (Fg) shows a negative correlation with AML patient prognosis, but mechanisms are unclear.
Purpose of the Study:
- To investigate the role of Fibrinogen in AML progression.
- To elucidate the molecular mechanisms underlying Fg's effect on AML.
Main Methods:
- Developed a Fg-deficient AML mouse model.
- Utilized AML cell lines and primary human AML cells for in vivo and in vitro studies.
Main Results:
- Fg significantly accelerates AML progression in xenograft and primary cell models.
- Fg upregulates miR-486-5p, which targets GPR153.
- This interaction activates the mTORC2/AKT pathway, promoting AML cell proliferation and migration.
Conclusions:
- Fg critically contributes to AML progression through the miR-486-5p/GPR153/mTORC2/AKT pathway.
- Fg represents a potential molecular target for AML therapeutic interventions.
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