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.