Running the Light: Nucleotide Metabolism Drives Bypass of Senescence in Cancer

Christopher J Halbrook; Daniel R Wahl; Costas A Lyssiotis

doi:10.1016/j.tibs.2019.10.007

Running the Light: Nucleotide Metabolism Drives Bypass of Senescence in Cancer

Trends Biochem Sci. 2019 Dec;44(12):991-993. doi: 10.1016/j.tibs.2019.10.007. Epub 2019 Nov 4.

Authors

Christopher J Halbrook¹, Daniel R Wahl², Costas A Lyssiotis³

Affiliations

¹ Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA.
² Department of Radiation Oncology, University of Michigan, Ann Arbor, MI, USA; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, USA.
³ Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI, USA; Rogel Cancer Center, University of Michigan, Ann Arbor, MI, USA; Department of Internal Medicine, Division of Gastroenterology and Hepatology, University of Michigan, Ann Arbor, MI, USA. Electronic address: clyssiot@med.umich.edu.

PMID: 31699584
DOI: 10.1016/j.tibs.2019.10.007

Abstract

Senescence is engaged in response to oncogenes to suppress proliferation. Cancers rewire metabolism to facilitate proliferation; however, it is not well appreciated how this enables senescence bypass. Recent work by Buj et al. demonstrates that loss of the tumor suppressor p16 engages a mTORC1-dependent increase in nucleotide pools to override senescence.

Keywords: RPIA; mTORC1; nucleotide metabolism; p16; pentose phosphate pathway.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Comment

MeSH terms

Cellular Senescence*
Humans
Mechanistic Target of Rapamycin Complex 1
Neoplasms / genetics*
Nucleotides
Oncogenes

Substances

Nucleotides
Mechanistic Target of Rapamycin Complex 1

Abstract

Publication types

MeSH terms

Substances

Grants and funding