Carcinogenesis and reactive oxygen species signaling: Interaction of the NADPH oxidase NOX1-5 and superoxide dismutase 1-3 signal transduction pathways

Research output: Contribution to journalReview article

7 Citations (Scopus)

Abstract

Significance: Reduction/oxidation (redox) balance could be defined as an even distribution of reduction and oxidation complementary processes and their reaction end products. There is a consensus that aberrant levels of reactive oxygen species (ROS), commonly observed in cancer, stimulate primary cell immortalization and progression of carcinogenesis. However, the mechanism how different ROS regulate redox balance is not completely understood. Recent Advances: In the current review, we have summarized the main signaling cascades inducing NADPH oxidase NOX1-5 and superoxide dismutase (SOD) 1-3 expression and their connection to cell proliferation, immortalization, transformation, and CD34+ cell differentiation in thyroid, colon, lung, breast, and hematological cancers. Critical Issues: Interestingly, many of the signaling pathways activating redox enzymes or mediating the effect of ROS are common, such as pathways initiated from G protein-coupled receptors and tyrosine kinase receptors involving protein kinase A, phospholipase C, calcium, and small GTPase signaling molecules. Future Directions: The clarification of interaction of signal transduction pathways could explain how cells regulate redox balance and may even provide means to inhibit the accumulation of harmful levels of ROS in human pathologies.

Original languageEnglish
Pages (from-to)443-486
Number of pages44
JournalAntioxidants and Redox Signaling
Volume30
Issue number3
DOIs
Publication statusPublished - Apr 5 2018

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Signal transduction
NADPH Oxidase
Superoxide Dismutase
Reactive Oxygen Species
Signal Transduction
Carcinogenesis
Oxidation
G-Protein-Coupled Receptor Kinases
Monomeric GTP-Binding Proteins
Receptor Protein-Tyrosine Kinases
Type C Phospholipases
Cyclic AMP-Dependent Protein Kinases
Protein-Tyrosine Kinases
Cell proliferation
Cell Differentiation
Pathology
Thyroid Gland
Colon
Cell Proliferation
Breast Neoplasms

Keywords

  • G proteincoupled receptor
  • NADPH oxidase NOX
  • redox signaling
  • superoxide dismutase
  • tyrosine kinase receptor

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Molecular Biology
  • Clinical Biochemistry
  • Cell Biology

Cite this

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title = "Carcinogenesis and reactive oxygen species signaling: Interaction of the NADPH oxidase NOX1-5 and superoxide dismutase 1-3 signal transduction pathways",
abstract = "Significance: Reduction/oxidation (redox) balance could be defined as an even distribution of reduction and oxidation complementary processes and their reaction end products. There is a consensus that aberrant levels of reactive oxygen species (ROS), commonly observed in cancer, stimulate primary cell immortalization and progression of carcinogenesis. However, the mechanism how different ROS regulate redox balance is not completely understood. Recent Advances: In the current review, we have summarized the main signaling cascades inducing NADPH oxidase NOX1-5 and superoxide dismutase (SOD) 1-3 expression and their connection to cell proliferation, immortalization, transformation, and CD34+ cell differentiation in thyroid, colon, lung, breast, and hematological cancers. Critical Issues: Interestingly, many of the signaling pathways activating redox enzymes or mediating the effect of ROS are common, such as pathways initiated from G protein-coupled receptors and tyrosine kinase receptors involving protein kinase A, phospholipase C, calcium, and small GTPase signaling molecules. Future Directions: The clarification of interaction of signal transduction pathways could explain how cells regulate redox balance and may even provide means to inhibit the accumulation of harmful levels of ROS in human pathologies.",
keywords = "G proteincoupled receptor, NADPH oxidase NOX, redox signaling, superoxide dismutase, tyrosine kinase receptor",
author = "Alessia Parascandolo and Laukkanen, {Mikko O.}",
year = "2018",
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T2 - Interaction of the NADPH oxidase NOX1-5 and superoxide dismutase 1-3 signal transduction pathways

AU - Parascandolo, Alessia

AU - Laukkanen, Mikko O.

PY - 2018/4/5

Y1 - 2018/4/5

N2 - Significance: Reduction/oxidation (redox) balance could be defined as an even distribution of reduction and oxidation complementary processes and their reaction end products. There is a consensus that aberrant levels of reactive oxygen species (ROS), commonly observed in cancer, stimulate primary cell immortalization and progression of carcinogenesis. However, the mechanism how different ROS regulate redox balance is not completely understood. Recent Advances: In the current review, we have summarized the main signaling cascades inducing NADPH oxidase NOX1-5 and superoxide dismutase (SOD) 1-3 expression and their connection to cell proliferation, immortalization, transformation, and CD34+ cell differentiation in thyroid, colon, lung, breast, and hematological cancers. Critical Issues: Interestingly, many of the signaling pathways activating redox enzymes or mediating the effect of ROS are common, such as pathways initiated from G protein-coupled receptors and tyrosine kinase receptors involving protein kinase A, phospholipase C, calcium, and small GTPase signaling molecules. Future Directions: The clarification of interaction of signal transduction pathways could explain how cells regulate redox balance and may even provide means to inhibit the accumulation of harmful levels of ROS in human pathologies.

AB - Significance: Reduction/oxidation (redox) balance could be defined as an even distribution of reduction and oxidation complementary processes and their reaction end products. There is a consensus that aberrant levels of reactive oxygen species (ROS), commonly observed in cancer, stimulate primary cell immortalization and progression of carcinogenesis. However, the mechanism how different ROS regulate redox balance is not completely understood. Recent Advances: In the current review, we have summarized the main signaling cascades inducing NADPH oxidase NOX1-5 and superoxide dismutase (SOD) 1-3 expression and their connection to cell proliferation, immortalization, transformation, and CD34+ cell differentiation in thyroid, colon, lung, breast, and hematological cancers. Critical Issues: Interestingly, many of the signaling pathways activating redox enzymes or mediating the effect of ROS are common, such as pathways initiated from G protein-coupled receptors and tyrosine kinase receptors involving protein kinase A, phospholipase C, calcium, and small GTPase signaling molecules. Future Directions: The clarification of interaction of signal transduction pathways could explain how cells regulate redox balance and may even provide means to inhibit the accumulation of harmful levels of ROS in human pathologies.

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