Basetti Madhu1, Masako Narita2, Masashi Narita2, John R. Griffiths1
1Molecular Imaging, Cancer Research UK Cambridge Research Institute, Cambridge, England, UK; 2Cellular Senescence & Tumour Suppressor Laboratory, Cancer Research UK Cambridge Research Institute, Cambridge, England, UK
Senescence, which is a permanent cell cycle arrest, is thought to act as a fail-safe mechanism to prevent the transformation of cells into malignant phenotypes; as a tumour suppressing mechanism it shares conceptual and therapeutic similarities with the apoptosis machinery. SA-β-gal activity, elevated p53 and p16 protein levels, coupled with morphological changes and gene expression, are used as senescence markers, though reliable metabolic markers for senescence are still required. We present a 1H NMR based metabolomics study of senescence induced by oncogenic Ras and etoposide-induced DNA damage, along with replicative senescence, quiescence and malignant transformation (by E1a/Ras) in HDFs
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