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S-adenosylhomocysteine hydrolase downregulation contributes to tumorigenesis

J F Leal1, I Ferrer, C Blanco-Aparicio

  • 1Spanish National Cancer Research Center (CNIO), 3 Melchor Fernández Almagro St, Madrid 28029, Spain.

Carcinogenesis
|August 21, 2008
PubMed

Insights

Researchers identified S-adenosylhomocysteine hydrolase (SAHH) as a potential tumor suppressor. SAHH inactivation promotes cell proliferation resistance and affects tumor suppressor gene activity, with reduced SAHH found in many human tumors.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Tumor suppressor genes are critical in preventing cancer development.
  • Genome-wide screens are essential for identifying novel genes involved in cell proliferation.
  • S-adenosylhomocysteine hydrolase (SAHH) was previously identified as a potential tumor suppressor.

Purpose of the Study:

  • To investigate the role of SAHH in cell proliferation and tumor suppression.
  • To determine the impact of SAHH inactivation on key cell cycle regulators like p53 and p21(Cip1).
  • To analyze SAHH expression patterns in human tumors.

Main Methods:

  • Genome-wide loss-of-function genetic screen.
  • Short hairpin RNA (shRNA) screening.
  • Analysis of p53 transcriptional activity and p21(Cip1) induction.
  • Quantitative analysis of SAHH mRNA and protein levels in tumor tissues.

Main Results:

  • SAHH inactivation confers resistance to p53 and p16(INK4)-induced proliferation arrest.
  • SAHH inactivation inhibits p53 transcriptional activity and impairs DNA damage-induced p21(Cip1) transcription.
  • SAHH mRNA was lost in 50% of diverse human tumor tissues analyzed.
  • SAHH protein levels were altered in some colon cancers.

Conclusions:

  • SAHH functions as a potential tumor suppressor by regulating cell proliferation and responding to DNA damage.
  • Downregulation of SAHH is a frequent event in human cancers.
  • SAHH represents a promising, yet largely unexplored, target for cancer research.

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