Hypoxia and Senescence: The Impact of Oxygenation on Tumor Suppression
- 15 May 2011
- journal article
- review article
- Published by American Association for Cancer Research (AACR) in Molecular Cancer Research
- Vol. 9 (5), 538-544
- https://doi.org/10.1158/1541-7786.mcr-11-0065
Abstract
Cellular senescence has emerged as a biological response to two major pathophysiological states of our being: cancer and aging. In the course of the transformation of a normal cell to a cancerous cell, senescence is frequently induced to suppress tumor development. In aged individuals, senescence is found in cells that have exhausted their replication potential. The similarity in these responses suggests that understanding how senescence is mediated can provide insight into both cancer and aging. One environmental factor that is implicated in both of these states is tissue hypoxia, which increases with aging and can inhibit senescence. Hypoxia is particularly important in normal physiology to maintain the stem cell niche; but at the same time, hypoxic inhibition of an essential tumor suppressor response can theoretically contribute to cancer initiation. Mol Cancer Res; 9(5); 538–44. ©2011 AACR.This publication has 87 references indexed in Scilit:
- Defining the role of hypoxia-inducible factor 1 in cancer biology and therapeuticsOncogene, 2009
- The H3K27me3 demethylase JMJD3 contributes to the activation of theINK4A–ARFlocus in response to oncogene- and stress-induced senescenceGenes & Development, 2009
- HIF-α Effects on c-Myc Distinguish Two Subtypes of Sporadic VHL-Deficient Clear Cell Renal CarcinomaCancer Cell, 2008
- Hyperoxia‐induced premature senescence requires p53 and pRb, but not mitochondrial matrix ROSThe FASEB Journal, 2008
- Telomere dysfunction and tumour suppression: the senescence connectionNature Reviews Cancer, 2008
- HIF-2α Promotes Hypoxic Cell Proliferation by Enhancing c-Myc Transcriptional ActivityCancer Cell, 2007
- Impaired DNA damage checkpoint response in MIF-deficient miceThe EMBO Journal, 2007
- Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replicationNature, 2006
- Plasminogen activator inhibitor-1 is a critical downstream target of p53 in the induction of replicative senescenceNature, 2006
- Oxygen sensitivity severely limits the replicative lifespan of murine fibroblastsNature, 2003