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

Aparna R Sertil, Alejandro P. Adam, Julio A. Aguirre-Ghiso

Research output: Contribution to journalArticle

66 Citations (Scopus)

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
StatePublished - Aug 15 2006
Externally publishedYes

Fingerprint

Tumors
Cells
Neoplasms
Growth
Modulation
Drug Resistance
Carcinoma
Pharmaceutical Preparations
Therapeutics

Keywords

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

ASJC Scopus subject areas

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Cite this

Opposing roles of mitogenic and stress signaling pathways in the induction of cancer dormancy. / Sertil, Aparna R; Adam, Alejandro P.; Aguirre-Ghiso, Julio A.

In: Cell Cycle, Vol. 5, No. 16, 15.08.2006, p. 1799-1807.

Research output: Contribution to journalArticle

Sertil, Aparna R ; Adam, Alejandro P. ; Aguirre-Ghiso, Julio A. / Opposing roles of mitogenic and stress signaling pathways in the induction of cancer dormancy. In: Cell Cycle. 2006 ; Vol. 5, No. 16. pp. 1799-1807.
@article{5946333289634c45b0db6f15a6d2457b,
title = "Opposing roles of mitogenic and stress signaling pathways in the induction of cancer dormancy",
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.",
keywords = "ERK, Metastasis, Microenvironment, p38, Quiescence, Tumor dormancy, Unfolded protein response, uPAR",
author = "Sertil, {Aparna R} and Adam, {Alejandro P.} and Aguirre-Ghiso, {Julio A.}",
year = "2006",
month = "8",
day = "15",
language = "English (US)",
volume = "5",
pages = "1799--1807",
journal = "Cell Cycle",
issn = "1538-4101",
publisher = "Landes Bioscience",
number = "16",

}

TY - JOUR

T1 - Opposing roles of mitogenic and stress signaling pathways in the induction of cancer dormancy

AU - Sertil, Aparna R

AU - Adam, Alejandro P.

AU - Aguirre-Ghiso, Julio A.

PY - 2006/8/15

Y1 - 2006/8/15

N2 - 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.

AB - 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.

KW - ERK

KW - Metastasis

KW - Microenvironment

KW - p38

KW - Quiescence

KW - Tumor dormancy

KW - Unfolded protein response

KW - uPAR

UR - http://www.scopus.com/inward/record.url?scp=33748923798&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33748923798&partnerID=8YFLogxK

M3 - Article

C2 - 16929185

AN - SCOPUS:33748923798

VL - 5

SP - 1799

EP - 1807

JO - Cell Cycle

JF - Cell Cycle

SN - 1538-4101

IS - 16

ER -