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NFATc1 regulates the transcription of DNA damage-induced apoptosis suppressor

Joo-Young Im1, Kang-Woo Lee2, Kyoung-Jae Won3

  • 1Genome Structure Research Center, KRIBB, Daejeon 305-806, Republic of Korea.

Data in Brief
|January 8, 2016
PubMed

Insights

DNA damage induced apoptosis suppressor (DDIAS) is highly expressed in lung cancers. Targeting DDIAS, regulated by NFATc1, offers a potential therapeutic strategy for lung cancer treatment.

Area of Science:

  • Molecular biology
  • Cancer research
  • Genetics

Background:

  • DNA damage induced apoptosis suppressor (DDIAS), also known as human Noxin (hNoxin), is significantly expressed in lung cancer tissues.
  • DDIAS plays a crucial role in cell survival, and its suppression can trigger apoptosis in cancer cells.

Purpose of the Study:

  • To investigate the transcriptional regulation of DDIAS.
  • To identify the transcription start site, promoter region, and key transcription factors involved in DDIAS expression.
  • To explore the therapeutic potential of targeting DDIAS in lung cancer.

Main Methods:

  • Cloning of the DDIAS promoter region.
  • Identification of transcription start site.
  • Analysis of transcription factor binding and regulation.

Main Results:

  • The transcription start site for DDIAS was identified at nucleotide 212 upstream of its translation start site.
  • NFAT2 was identified as a major transcription factor regulating DDIAS.
  • NFATc1 was demonstrated to regulate DDIAS expression in both pancreatic and lung cancer cell lines.

Conclusions:

  • DDIAS is a key regulator of apoptosis and is upregulated in lung cancer.
  • NFATc1 is a critical transcription factor controlling DDIAS expression, presenting a potential therapeutic target.
  • Understanding DDIAS regulation provides insights for developing novel lung cancer therapies.
Keywords:
ChIPDDIASLung cancerNFATc1Pancreatic cancer

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