Journal Article

<i>S-adenosylhomocysteine hydrolase</i> downregulation contributes to tumorigenesis

J.F. Leal, I. Ferrer, C. Blanco-Aparicio, J. Hernández-Losa, S. Ramón y Cajal, A. Carnero and M.E. LLeonart

in Carcinogenesis

Volume 29, issue 11, pages 2089-2095
Published in print November 2008 | ISSN: 0143-3334
Published online August 2008 | e-ISSN: 1460-2180 | DOI:
S-adenosylhomocysteine hydrolase downregulation contributes to tumorigenesis

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With the idea to discover novel genes involved in proliferation, we have performed a genome-wide loss-of-function genetic screen to identify additional putative tumor suppressor genes. We have previously identified five genes belonging to different biochemical families. In this report, we focused on the study of one of these genes designated S-adenosylhomocysteine hydrolase (SAHH), which has also been previously identified in an independent short hairpin RNA screening. SAHH inactivation confers resistance to both p53 and p16INK4-induced proliferation arrest. Interestingly, SAHH inactivation inhibits p53 transcriptional activity and impairs DNA damage-induced transcription of p21Cip1. Given that SAHH downregulation modulates senescence in primary cells, we also studied SAHH expression in human tumors at the messenger RNA (mRNA) and protein levels. SAHH mRNA was lost in 50% of tumor tissues from 206 patients with different kinds of tumors in comparison with normal tissue counterparts. Moreover, SAHH protein was also affected in some colon cancers. Such findings may be of relevance to cancer research, suggesting that SAHH might be a largely unexplored tumor suppressor.

Journal Article.  5759 words.  Illustrated.

Subjects: Clinical Cytogenetics and Molecular Genetics

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