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ATRX Knockdown Enhances Irradiation-Induced Mitotic Catastrophe in p53-Deficient Cancer Cells

Lijing Qin1,2, Rongrong Liu1, Weiqiang Xu1

  • 1NHC Key Laboratory of Radiobiology, School of Public Health, JilinUniversity, Changchun, Jilin, China.

Cell Biology International
|May 9, 2026
PubMed

Insights

Knocking down Alpha-thalassemia/mental retardation syndrome X-linked (ATRX) protein promotes irradiation-induced mitotic catastrophe (MC) in p53-deficient and p53-mutant cancer cells. This occurs via downregulation of spindle assembly checkpoint and chromosomal passenger complex proteins.

Area of Science:

  • Oncology
  • Cell Biology
  • Genetics

Background:

  • Mitotic catastrophe (MC) is a tumor suppressor mechanism crucial for genomic stability.
  • Alpha-thalassemia/mental retardation syndrome X-linked (ATRX) is vital for DNA replication, repair, and maintaining mitosis.
  • The impact of ATRX knockdown on radiation-induced MC is not fully understood.

Purpose of the Study:

  • To investigate the effects of ATRX knockdown (KD) on irradiation-induced MC.
  • To elucidate the underlying mechanisms of ATRX KD in various p53 contexts (wild-type, deficient, mutant).

Main Methods:

  • Utilized p53-wild type, p53-deficient, and p53-mutant cancer cell lines.
  • Administered irradiation and performed ATRX knockdown.
  • Analyzed cell cycle progression, MC characteristics, and protein expression (spindle assembly checkpoint, chromosomal passenger complex).

Main Results:

  • Irradiation caused G2/M arrest in all cell types.
  • ATRX KD induced G1 arrest and S phase delay in irradiated HCT116 p53+/+ cells.
  • ATRX KD triggered MC specifically in p53-deficient (HCT116 p53-/-) and p53-mutant (MDA-MB-231) cells, not p53-proficient cells.
  • This was linked to reduced spindle assembly checkpoint and chromosomal passenger complex proteins.

Conclusions:

  • ATRX KD exacerbates irradiation-induced MC in p53-deficient and mutant cancer cells.
  • The mechanism involves downregulation of SAC and CPC proteins.
  • This enhances radiation-induced proliferation inhibition and apoptosis in p53-deficient cells.
Keywords:
ATRXapoptosisionizing radiationmitotic catastrophep53

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