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TYMS promotes genomic instability and tumor progression in Ink4a/Arf null background.

Maria V Guijarro1, Akbar Nawab1, Peter Dib1

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Elevated thymidylate synthase (TYMS) expression combined with Ink4a/Arf loss accelerates cancer development and metastasis in mice. Targeting TYMS shows promise for delaying tumor growth and improving survival.

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Area of Science:

  • Oncology
  • Cancer Biology
  • Genetics

Background:

  • Elevated thymidylate synthase (TYMS) expression is linked to oncogenesis and tumorigenesis.
  • Loss of Ink4a/Arf is a frequent somatic mutation in human cancers.
  • Understanding gene cooperation in cancer development is crucial.

Purpose of the Study:

  • To investigate the cooperative effect of ectopic human TYMS expression and Ink4a/Arf loss on tumorigenesis.
  • To determine the impact of this cooperation on tumor progression, metastasis, and genomic stability.
  • To evaluate the therapeutic potential of targeting TYMS in this context.

Main Methods:

  • Utilized a genetically engineered mouse model with human TYMS and Ink4a/Arf deficiency (hTS/Ink4a/Arf -/-).
  • Assessed tumor incidence, progression, metastasis, and survival rates.
  • Analyzed genomic instability markers, including DNA damage and aneuploidy.
  • Investigated the effect of TYMS downregulation in vitro and in vivo using shRNA.

Main Results:

  • Deregulated TYMS expression in an Ink4a/Arf null background accelerated tumorigenesis and metastasis.
  • Tumors exhibited genomic instability, increased DNA damage, aneuploidy, and G1/S checkpoint loss.
  • In vitro TYMS downregulation reduced proliferation and sensitized cells to chemotherapy.
  • In vivo TYMS depletion reduced tumor incidence, delayed progression, and prolonged survival.

Conclusions:

  • Cooperation between TYMS activation and Ink4a/Arf loss enhances uncontrolled cell proliferation and tumor growth.
  • Targeting TYMS is a promising strategy to delay tumorigenesis and prolong survival in relevant cancer contexts.
  • This study highlights the importance of targeting specific genetic interactions in cancer therapy.