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Related Experiment Video

Updated: Jun 23, 2025

Isolation of Primary Cancer-Associated Fibroblasts from a Syngeneic Murine Model of Breast Cancer for the Study of Targeted Nanoparticles

Isolation of Primary Cancer-Associated Fibroblasts from a Syngeneic Murine Model of Breast Cancer for the Study of Targeted Nanoparticles

Published on: May 14, 2021

Dotting Out AML by Targeting Fibrillarin.

Hanzhi Luo¹, Michael G Kharas¹

¹Molecular Pharmacology Program, Center for Cell Engineering, Center for Stem Cell Biology, Center for Experimental Therapeutics, Center for Hematologic Malignancies, Memorial Sloan Kettering Cancer Center, New York, New York.

Cancer Research

|June 26, 2024

Summary

Fibrillarin (FBL) drives acute myeloid leukemia (AML) by regulating ribosome biogenesis. Targeting FBL

Area of Science:

Biochemistry
Molecular Biology
Oncology

Background:

Biomolecular condensates are increasingly recognized as drivers of tumorigenesis.
In acute myeloid leukemia (AML), RNA-binding protein condensates dysregulate transcriptional networks.

Purpose of the Study:

To investigate the role of fibrillarin (FBL) in AML leukemogenesis.
To explore FBL's phase separation properties as a potential therapeutic target.

Main Methods:

CRISPR screening to identify FBL as an AML driver.
Assessing the impact of FBL depletion on AML cell cycle and survival.
Investigating FBL's role in pre-ribosomal RNA (pre-rRNA) processing and ribosome biogenesis.
Evaluating the therapeutic efficacy of CGX-635 targeting FBL.

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Main Results:

FBL depletion induced cell cycle arrest and death in AML cells with minimal effect on normal cells.
FBL's phase separation domains are crucial for pre-rRNA processing and AML cell survival.
FBL regulates ribosome biogenesis and translation of oncogenic proteins like MYC.
The chemotherapeutic agent CGX-635 targets FBL, impairing pre-rRNA processing and reducing AML cell survival.

Conclusions:

FBL's phase separation is a critical vulnerability in AML.
Targeting RNA-binding protein phase separation offers a novel therapeutic strategy for AML.
Further research into condensate dynamics and condensate-modulating drugs holds promise for cancer therapy.