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Frequent somatic mutations of the transcription factor ATBF1 in human prostate cancer

Xiaodong Sun1, Henry F Frierson, Ceshi Chen

  • 1Winship Cancer Institute, Department of Hematology and Oncology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

Nature Genetics
|March 8, 2005
PubMed

Insights

The AT-binding factor 1 (ATBF1) gene, located on chromosome 16q22, is frequently altered in prostate cancer. Loss of ATBF1 function contributes to uncontrolled cell growth, identifying it as a potential tumor suppressor.

Area of Science:

  • Genetics
  • Molecular Biology
  • Oncology

Background:

  • Cancer development involves accumulating genetic alterations.
  • The tumor suppressor gene targeted by 16q22 deletions in human cancers remains unidentified.
  • ATBF1 is a transcription factor regulating AFP, MYB, and CDKN1A.

Purpose of the Study:

  • To identify the tumor suppressor gene responsible for 16q22 deletions in human cancers.
  • To investigate the role of ATBF1 in prostate cancer development.

Main Methods:

  • Deletion mapping to narrow down the 16q22 region to 861 kb containing ATBF1.
  • Analysis of ATBF1 mRNA levels in normal and cancerous prostate tissues.
  • Somatic mutation analysis of the ATBF1 gene in prostate cancer samples.
  • Assessment of ATBF1's effect on cell proliferation.

Main Results:

  • ATBF1 was identified as a candidate tumor suppressor gene at 16q22.
  • ATBF1 mRNA levels were reduced in approximately 50% of prostate cancers.
  • 22 unique somatic mutations in ATBF1 were found in 36% of prostate cancers, many impairing its function.
  • ATBF1 demonstrated inhibition of cell proliferation.

Conclusions:

  • Loss of ATBF1 function is a mechanism contributing to uncontrolled cell proliferation in prostate cancer.
  • ATBF1 acts as a tumor suppressor gene at the 16q22 locus.
  • These findings highlight the significance of ATBF1 in prostate tumorigenesis.

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