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December 8, 2025BloodOpen Access

FBXO3-mediated DUSP9 ubiquitination reprograms MAPK signaling to eradicate tyrosine kinase inhibitor-resistant CML stem cells

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Authors

XLXudong LiRXRongfeng XuYSYongping Song

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Overview

Experimental data shows FBXO3 regulates proliferation and apoptosis in leukemic stem cells, implicating new treatment avenues.

Key Points

  • To investigate the role of FBXO3 in chronic myeloid leukemia stem cells and its therapeutic implications.
  • Used single-cell RNA sequencing to assess FBXO3 expression in CML patients vs healthy individuals.
  • Inhibited FBXO3 using shRNA and sgRNA in CML cell lines to evaluate effects on growth and apoptosis.
  • Established CML tumor models to evaluate FBXO3's role in vivo and screened candidate substrate proteins for ubiquitination.
  • FBXO3 expression is elevated in CML patients, correlating with patient data.
  • Silencing FBXO3 reduced growth and increased apoptosis in CML cell lines and CD34+ cells.
  • FBXO3 inhibition in mouse models lowered leukemia burden and prolonged survival without harming normal stem cells.

Cite This Study

Li et al. (2025) studied this question.

synapsesocial.com/papers/693624d74fa91c937236d0ddhttps://doi.org/10.1182/blood-2025-3754
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