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MUC1-C Oncoprotein Interacts Directly with ATM and Promotes the DNA Damage Response to Ionizing Radiation

Lei Huang1, Xiaodong Liao, Michael Beckett

  • 1Model Organism Division, Department of Medical Genetics, E-Institutes of Shanghai Universities, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, P.R. China.

Genes & Cancer
|September 25, 2010
PubMed

Insights

MUC1 oncoprotein interacts with ATM kinase, aiding DNA repair and protecting breast cancer cells from radiation damage. This interaction helps repair DNA double-strand breaks, reducing cell death and chromosomal damage.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cellular Response to DNA Damage

Background:

  • Ataxia-telangiectasia mutated (ATM) kinase is crucial for DNA double-strand break (DSB) repair following ionizing radiation (IR).
  • MUC1 oncoprotein is overexpressed in human breast carcinomas, suggesting a role in cancer progression.

Purpose of the Study:

  • To investigate the interaction between MUC1 C-terminal subunit (MUC1-C) and ATM in breast cancer cells.
  • To determine the functional significance of MUC1-C and ATM interaction in response to IR-induced DNA damage.

Main Methods:

  • Co-immunoprecipitation assays to demonstrate MUC1-C and ATM interaction.
  • In vitro binding assays to map MUC1-C domain interaction with ATM HEAT repeats.
  • Immunofluorescence microscopy to track γH2AX foci removal.
  • Analysis of chromosomal aberrations and cell death post-IR exposure.

Main Results:

  • MUC1-C constitutively interacts with ATM in human breast cancer cells.
  • MUC1-C directly binds to ATM HEAT repeats and the ATM substrate H2AX.
  • MUC1-C promotes the removal of IR-induced nuclear γH2AX foci.
  • MUC1-C protects against IR-induced chromosomal aberrations and cell death by enhancing DNA repair.

Conclusions:

  • MUC1-C interaction with ATM plays a significant role in DNA repair and cell survival following IR.
  • Overexpressed MUC1 may exploit DNA repair pathways to protect malignant cells from radiation-induced damage.
  • Targeting MUC1-C-ATM interaction could be a therapeutic strategy for breast cancer treatment.

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