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Novel function of transcription factor ATF5: blockade of p53-dependent apoptosis induced by ionizing irradiation

Takeshi Nishioka1, Yusuke Miyai, Hisashi Haga

  • 1Department of Biomedical Sciences and Engineering, Faculty of Health Sciences, Graduate School of Health Sciences, Hokkaido University, Sapporo, Japan. trout@hs.hokudai.ac.jp

Cell Structure and Function
|March 19, 2009
PubMed
Abstract

Insights

The transcription factor ATF5 represses p53 activity, influencing tumor radioresistance and cell motility. Restoring ATF5 in radiosensitive cells enhances resistance to radiation and p53-induced cell death.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • p53 is a critical tumor suppressor involved in DNA repair and apoptosis.
  • Radiosensitivity is a key factor in cancer treatment efficacy.
  • Understanding molecular mechanisms regulating radiosensitivity is crucial for improving cancer therapy.

Purpose of the Study:

  • To identify novel molecules modulating p53-dependent radiosensitivity.
  • To investigate the role of transcription factor ATF5 in radioresistance.

Main Methods:

  • Utilized mouse sarcoma cell lines (QRsP(p53+/+)) to establish radiosensitive and radioresistant clones.
  • Employed colony assays, p53 gene transfer, luciferase assays (for p53 and p21), animal transplantation, and DNA array analyses.
  • Performed flow cytometry and time-lapse cell migration observations.

Main Results:

  • Microarray analysis revealed reduced ATF5 expression in radiosensitive clones.
  • ATF5 was found to suppress the transactivational activity of p53 and p63.
  • ATF5 gene transfer restored radioresistance and reduced Ad-p53-induced apoptosis in radiosensitive cells.
  • Increased cell motility was observed in ATF5-transfected radiosensitive cells.

Conclusions:

  • ATF5 acts as a potent repressor of p53.
  • Elevated ATF5 expression in tumors may correlate with enhanced malignant phenotypes like radioresistance and increased cell motility.

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