Basetti Madhu1, Masako Narita2, Masashi Narita2, John R. Griffiths1
1Molecular Imaging, Cancer Research UK Cambridge Research Institute, Cambridge, England, United Kingdom; 2Cellular Senescence and Tumour Suppressor Lab, Cancer Research UK Cambridge Research Institute, Cambridge, England, United Kingdom
Senescence, a permanent cell cycle arrest, is thought to be a fail-safe mechanism that prevents the malignant transformation of cells; 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 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 or MEK, or by prolonged replication, compared with growing, transformed, and quiescent cells. The data shows that phosphocholine/glycerophosphocholine ratio is a potential metabolic marker for cellular senescence.