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CTCF puts a new twist on UV damage and repair in skin cancer

Bastian Stark1, Gregory M K Poon2, John J Wyrick1,3

  • 1School of Molecular Biosciences, Washington State University, Pullman, WA, USA.

Molecular & Cellular Oncology
|April 14, 2022
PubMed

Insights

CCCTC-binding factor (CTCF) binding sites in skin cancer DNA are prone to UV damage. This damage, combined with inhibited repair, drives mutations, explaining cancer development.

Area of Science:

  • Genetics
  • Molecular Biology
  • Dermatology

Background:

  • Somatic mutations are key drivers of skin cancer development.
  • CCCTC-binding factor (CTCF) is a known regulator of genome architecture.
  • Mutations in skin cancer are not randomly distributed, suggesting underlying mechanisms.

Purpose of the Study:

  • To investigate the role of CTCF binding sites in skin cancer mutagenesis.
  • To understand how CTCF binding influences DNA susceptibility to UV damage.
  • To elucidate the mechanisms linking CTCF, UV damage, and mutation formation.

Main Methods:

  • Analysis of mutation patterns in skin cancer genomes.
  • Experimental assessment of DNA structure and UV damage at CTCF sites.
  • Investigation of DNA repair dynamics at CTCF-bound regions.

Main Results:

  • Somatic mutations in skin cancers are significantly enriched at CTCF binding sites.
  • CTCF binding alters DNA structure, increasing susceptibility to UV-induced damage.
  • DNA repair is inhibited at these damaged CTCF sites, promoting mutagenesis.

Conclusions:

  • CTCF binding plays a critical role in shaping the mutation landscape of skin cancer.
  • The interplay between CTCF, UV damage, and impaired repair is a major mechanism of UV mutagenesis.
  • Targeting these processes could offer new strategies for skin cancer prevention and treatment.
Keywords:
CCCTC-binding factorDNA repairUltraviolet lightskin cancertranscription factor

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