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Claspin haploinsufficiency leads to defects in fertility, hyperplasia and an increased oncogenic potential

Suzanne Madgwick1, Saimir Luli2, Helene Sellier1

  • 1Newcastle University Biosciences Institute, Wolfson Childhood Cancer Research Centre, Level 6, Herschel Building, Newcastle University, Brewery Lane, Newcastle upon Tyne NE1 7RU, U.K.

The Biochemical Journal
|October 14, 2022
PubMed

Insights

Reduced Claspin protein levels impair fertility and promote liver disease and cancer. This study reveals Claspin

Area of Science:

  • Cellular biology
  • Molecular biology
  • Genetics

Background:

  • Claspin is an adaptor protein crucial for DNA replication stress response.
  • Variable Claspin expression in cancer correlates with patient survival.
  • The biological impact of reduced Claspin levels remains largely unknown.

Purpose of the Study:

  • To investigate the consequences of heterozygous Clspn gene knockout.
  • To determine the role of Claspin in tumorigenesis and disease.

Main Methods:

  • Generation and analysis of Clspn+/- mice.
  • Assessment of fertility, oocyte meiosis, and age-related pathologies.
  • Evaluation of liver damage and hepatocellular carcinoma development using the DEN model.

Main Results:

  • Claspin haploinsufficiency caused reduced female fertility and meiotic defects.
  • Aged Clspn+/- mice exhibited lymphoid hyperplasia and increased susceptibility to fatty liver disease.
  • Reduced Claspin levels exacerbated liver damage and promoted hepatocellular carcinoma in the DEN model.

Conclusions:

  • Claspin haploinsufficiency has diverse, unexpected biological effects.
  • Claspin acts as a tumor suppressor, regulating tumorigenesis and multiple disease etiologies.
  • These findings highlight Claspin's critical role in maintaining organismal health and preventing cancer.
Keywords:
ClapsinDNA replication and recombinationgenome integrityhepatocellular carcinomahyperplasiaoocyte

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