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Mithramycin A Enhances Tumor Sensitivity to Mitotic Catastrophe Resulting From DNA Damage

Bradley T Scroggins1, Jeffrey Burkeen1, Ayla O White1

  • 1Radiation Oncology Branch, National Institutes of Health, Bethesda, Maryland.

International Journal of Radiation Oncology, Biology, Physics
|November 22, 2017
PubMed
Abstract

Insights

Mithramycin A (MTA) enhances radiation therapy effectiveness by inhibiting Specificity Protein 1 (SP1) in tumor cells. This SP1 inhibition sensitizes cancer cells to radiation, leading to improved tumor growth delay in preclinical models.

Area of Science:

  • Oncology
  • Molecular Biology
  • Radiation Oncology

Background:

  • Specificity Protein 1 (SP1) is a transcription factor crucial for maintaining tumor growth.
  • Understanding SP1's role is key to developing novel cancer treatment strategies.

Purpose of the Study:

  • To investigate the effects of mithramycin A (MTA), an SP1 inhibitor, on the response of tumor cells to radiation therapy.
  • To evaluate MTA's potential as a radiosensitizer in human tumor models.

Main Methods:

  • Assessed clonogenic survival and DNA damage repair (γH2AX foci) in A549 and UM-UC-3 cells treated with MTA and irradiation.
  • Evaluated mitotic catastrophe, gene expression via PCR arrays, and in vivo tumor growth delay in xenograft models.

Main Results:

  • MTA sensitized A549 and UM-UC-3 cells to irradiation, increasing mitotic catastrophe and suppressing cell death genes.
  • MTA treatment enhanced radiation-induced tumor growth delay in vivo without affecting DNA damage repair.
  • No significant effect on radiation response was observed in human fibroblasts (BJ cells).

Conclusions:

  • SP1 is a viable target for enhancing radiation therapy efficacy.
  • Mithramycin A demonstrates potential as a clinical radiation sensitizer for human tumors.

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