A new component of the mammalian cellular defence mechanism against tumour production is identified in a report in the 02 Dec 2004 issue of Nature (Vol. 432, No. 7017, pp. 639-645). The gene involved, Seladin-1, is somewhat of a surprise package, as it has previously been linked to Alzheimer's disease and cholesterol metabolism.
Expression of oncogenes can lead to the generation of cancer cells; faced with this threat, a cellular senescence (cell ageing) programme kicks in, which is thought to be a weapon in the fight against tumorigenesis. By carrying out a genetic screen, Konstantin Galaktionov and colleagues found that Seladin-1 mediates senescence induced by the protein Ras. Knocking out Seladin-1 side-stepped Ras-induced senescence in rat and human fibroblast cells, allowing the cells to become cancerous as a result of unregulated Ras activity. An interaction between Seladin-1 and the tumour suppressor p53, initiated by oncogenic and oxidative stress, lies at the heart of this regulatory effect of Seladin-1.
Konstantin Galaktionov (Baylor College of Medicine, Houston, TX, USA)
Tel: +1 713 798 8280, E-mail: firstname.lastname@example.org
(C) Nature press release.
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