Related Experiment Video

Updated: Mar 23, 2026

Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay
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Detection and Visualization of DNA Damage-induced Protein Complexes in Suspension Cell Cultures Using the Proximity Ligation Assay

Published on: June 9, 2017

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Cancer-associated SF3B1 mutation suppresses DNA repair by disrupting the organization of nuclear actin network

Rui Qian1,2, Zhipeng Zhao3, Xuanxuan Sun1

  • 1Cancer Biology Laboratory, China-Japan Union Hospital of Jilin University, Jilin University, Changchun, China.

Cell Death & Disease
|March 22, 2026
PubMed

Insights

SF3B1 mutation impairs DNA repair by disrupting the nuclear actin network. This involves circATP9B, MYH9 degradation, and suppressed DNA damage foci movement, impacting cancer progression.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • Nuclear actin filaments are crucial for efficient DNA double-strand break repair.
  • Cancer-associated SF3B1 mutations are linked to impaired DNA repair, but the mechanism is unclear.

Purpose of the Study:

  • To elucidate the mechanism by which SF3B1 mutations impair DNA repair.
  • To investigate the role of nuclear actin organization in DNA repair and cancer progression.

Main Methods:

  • Investigated the effect of SF3B1 mutation on nuclear actin network formation during DNA repair.
  • Analyzed the role of circATP9B and MYH9 in the SF3B1-mediated DNA repair pathway.
  • Assessed the impact of MYH9 deficiency on DNA damage foci dynamics and repair efficiency.

Main Results:

  • SF3B1 mutation leads to a defective nuclear actin network during DNA repair.
  • SF3B1 mutation increases circATP9B expression, causing MYH9 degradation.
  • MYH9 deficiency disrupts nuclear actin assembly, hindering DNA damage foci movement and repair.

Conclusions:

  • SF3B1 mutation impairs DNA repair via a circATP9B-MYH9-actin pathway, influencing cancer progression.
  • MYH9 is essential for organizing the nuclear actin network required for efficient DNA repair.

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