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Redox signaling at invasive microdomains in cancer cells
被引:31
|作者:
Diaz, Begona
[1
]
Courtneidge, Sara A.
[1
]
机构:
[1] Sanford Burnham Med Res Inst, Ctr Canc, La Jolla, CA 92037 USA
关键词:
Redox;
ROS;
Signaling;
Cancer;
Migration;
Invasion;
Invadopodia;
NADPH oxidase;
Tks4;
Tks5;
Nox4;
Nox1;
p22phox;
PTPs;
Free radicals;
PROTEIN-TYROSINE-PHOSPHATASE;
EXTRACELLULAR-MATRIX DEGRADATION;
CHRONIC GRANULOMATOUS-DISEASE;
SPECIALIZED SURFACE PROTRUSIONS;
ENDOTHELIAL GROWTH-FACTOR;
SMOOTH-MUSCLE-CELLS;
REACTIVE OXYGEN;
NADPH OXIDASE;
PX DOMAIN;
REVERSIBLE INACTIVATION;
D O I:
10.1016/j.freeradbiomed.2011.09.016
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Redox signaling contributes to the regulation of cancer cell proliferation, survival, and invasion and participates in the adaptation of cancer cells to their microenvironment. NADPH oxidases are important mediators of redox signaling in normal and cancer cells. Redox signal specificity in normal cells is in part achieved by targeting enzymes that generate reactive oxygen species to specific subcellular microdomains such as focal adhesions, dorsal ruffles, lipid rafts, or caveolae. In a similar fashion, redox signal specificity during cancer cell invasion can be regulated by targeting reactive oxygen generation to invasive microdomains such as invadopodia. Here we summarize recent advances in the understanding of the redox signaling processes that control the cancer cell proinvasive program by modulating cell adhesion, migration, and proteolysis as well as the interaction of cancer cells with the tumor microenvironment. We focus on redox signaling events mediated by invadopodia NADPH oxidase complexes and their contribution to cancer cell invasion. (C) 2011 Elsevier Inc. All rights reserved.
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页码:247 / 256
页数:10
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