Related Experiment Video

Updated: May 8, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
10:21

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.

Haematologica
|May 7, 2026
PubMed

Insights

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.

More Related Videos

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line06:24

Oncogene Expression Analysis with Alterations in pH in a Pancreatic Ductal Cell Line

Published on: April 11, 2025

Related Concept Videos

Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...