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SIRT1 promotes thyroid carcinogenesis driven by PTEN deficiency

D Herranz1, A Maraver, M Cañamero

  • 1Tumor Suppression Group, Spanish National Cancer Research Center (CNIO), Madrid, Spain.

Oncogene
|September 19, 2012
PubMed

Insights

SIRT1, previously thought to suppress tumors, acts as an oncogene in mouse thyroid and prostate cancers by increasing c-MYC. This finding suggests SIRT1 as a potential therapeutic target for thyroid carcinomas.

Area of Science:

  • Molecular Biology
  • Oncology
  • Genetics

Background:

  • SIRT1 is generally considered a tumor suppressor based on mouse models.
  • Previous research has not identified oncogenic roles for SIRT1 in vivo.

Purpose of the Study:

  • To investigate the role of SIRT1 in Pten-deficient murine thyroid and prostate carcinogenesis.
  • To determine the relationship between SIRT1 and c-MYC in cancer development.

Main Methods:

  • Transgenic mouse models with Sirt1 overexpression were used.
  • mRNA expression analysis and Western blotting were performed on murine tissues and cultured cells.
  • Correlation analysis was conducted between SIRT1 and c-MYC levels in human thyroid cancers.

Main Results:

  • Transgenic Sirt1 expression promoted thyroid and prostate carcinogenesis in Pten-deficient mice.
  • SIRT1 overexpression led to increased c-MYC transcription and protein levels in murine thyroid tumors.
  • SIRT1 was overexpressed in human thyroid cancers and positively correlated with c-MYC protein levels.
  • SIRT1 was found to stabilize c-MYC protein in cultured thyroid cancer cells.

Conclusions:

  • SIRT1 exhibits oncogenic activity in specific cancer contexts, contrary to previous assumptions.
  • SIRT1 promotes cancer progression by upregulating c-MYC.
  • SIRT1 represents a potential therapeutic target for thyroid carcinomas.

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