Opposing roles of mitogenic and stress signaling pathways in the induction of cancer dormancy

Aparna C. Ranganathan, Alejandro P. Adam, Julio A. Aguirre-Ghiso

Research output: Contribution to journalReview article

67 Scopus citations

Abstract

Cancer dormancy is a poorly understood stage of cancer progression. However, the ability to control this step of the disease offers novel therapeutic opportunities. Here we summarize recent findings that implicate the extracellular matrix and adhesion receptor signaling in the escape or induction of tumor dormancy. We further review evidence suggesting that imbalances in the activity ratio of ERK to p38 signaling may determine the fate (i.e., tumorigenicity vs. dormancy) of different carcinoma cells. Special attention is placed on the mechanisms that p38 signaling regulates during the induction of dormancy and how modulation of these pathways may offer a therapeutic opportunity. We also review evidence for a novel drug-resistance mechanism in dormant tumor cells that when blocked may enable killing of dormant tumor cells. Finally, we explore the notion that dormancy of tumor cells may be the result of a selective adaptive response that allows disseminated tumor cells to pause their growth and cope with stress signaling imposed by dissemination and/or treatment until growth can be restored.

Original languageEnglish (US)
Pages (from-to)1799-1807
Number of pages9
JournalCell Cycle
Volume5
Issue number16
DOIs
StatePublished - Aug 15 2006

Keywords

  • ERK
  • Metastasis
  • Microenvironment
  • Quiescence
  • Tumor dormancy
  • Unfolded protein response
  • p38
  • uPAR

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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