42 Citations (Scopus)

Abstract

The interplay between Ca2+ and reactive oxygen species (ROS) signaling pathways is well established, with reciprocal regulation occurring at a number of subcellular locations. Many Ca2+ channels at the cell surface and intracellular organelles, including the endoplasmic reticulum and mitochondria are regulated by redox modifications. In turn, Ca2+ signaling can influence the cellular generation of ROS, from sources such as NADPH oxidases and mitochondria. This relationship has been explored in great depth during the process of apoptosis, where surges of Ca2+ and ROS are important mediators of cell death. More recently, coordinated and localized Ca2+ and ROS transients appear to play a major role in a vast variety of pro-survival signaling pathways that may be crucial for both physiological and pathophysiological functions. While much work is required to firmly establish this Ca2+-ROS relationship in cancer, existing evidence from other disease models suggests this crosstalk is likely of significant importance in tumorigenesis. In this review, we describe the regulation of Ca2+ channels and transporters by oxidants and discuss the potential consequences of the ROS-Ca2+ interplay in tumor cells.

Original languageEnglish (US)
Pages (from-to)70-96
Number of pages27
JournalCell Calcium
Volume63
DOIs
StatePublished - May 1 2017

Fingerprint

Reactive Oxygen Species
Calcium
Neoplasms
Mitochondria
NADPH Oxidase
Oxidants
Endoplasmic Reticulum
Organelles
Oxidation-Reduction
Carcinogenesis
Cell Death
Apoptosis

All Science Journal Classification (ASJC) codes

  • Physiology
  • Molecular Biology
  • Cell Biology

Cite this

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title = "Crosstalk between calcium and reactive oxygen species signaling in cancer",
abstract = "The interplay between Ca2+ and reactive oxygen species (ROS) signaling pathways is well established, with reciprocal regulation occurring at a number of subcellular locations. Many Ca2+ channels at the cell surface and intracellular organelles, including the endoplasmic reticulum and mitochondria are regulated by redox modifications. In turn, Ca2+ signaling can influence the cellular generation of ROS, from sources such as NADPH oxidases and mitochondria. This relationship has been explored in great depth during the process of apoptosis, where surges of Ca2+ and ROS are important mediators of cell death. More recently, coordinated and localized Ca2+ and ROS transients appear to play a major role in a vast variety of pro-survival signaling pathways that may be crucial for both physiological and pathophysiological functions. While much work is required to firmly establish this Ca2+-ROS relationship in cancer, existing evidence from other disease models suggests this crosstalk is likely of significant importance in tumorigenesis. In this review, we describe the regulation of Ca2+ channels and transporters by oxidants and discuss the potential consequences of the ROS-Ca2+ interplay in tumor cells.",
author = "Nadine Hempel and Mohamed Trebak",
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Crosstalk between calcium and reactive oxygen species signaling in cancer. / Hempel, Nadine; Trebak, Mohamed.

In: Cell Calcium, Vol. 63, 01.05.2017, p. 70-96.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Crosstalk between calcium and reactive oxygen species signaling in cancer

AU - Hempel, Nadine

AU - Trebak, Mohamed

PY - 2017/5/1

Y1 - 2017/5/1

N2 - The interplay between Ca2+ and reactive oxygen species (ROS) signaling pathways is well established, with reciprocal regulation occurring at a number of subcellular locations. Many Ca2+ channels at the cell surface and intracellular organelles, including the endoplasmic reticulum and mitochondria are regulated by redox modifications. In turn, Ca2+ signaling can influence the cellular generation of ROS, from sources such as NADPH oxidases and mitochondria. This relationship has been explored in great depth during the process of apoptosis, where surges of Ca2+ and ROS are important mediators of cell death. More recently, coordinated and localized Ca2+ and ROS transients appear to play a major role in a vast variety of pro-survival signaling pathways that may be crucial for both physiological and pathophysiological functions. While much work is required to firmly establish this Ca2+-ROS relationship in cancer, existing evidence from other disease models suggests this crosstalk is likely of significant importance in tumorigenesis. In this review, we describe the regulation of Ca2+ channels and transporters by oxidants and discuss the potential consequences of the ROS-Ca2+ interplay in tumor cells.

AB - The interplay between Ca2+ and reactive oxygen species (ROS) signaling pathways is well established, with reciprocal regulation occurring at a number of subcellular locations. Many Ca2+ channels at the cell surface and intracellular organelles, including the endoplasmic reticulum and mitochondria are regulated by redox modifications. In turn, Ca2+ signaling can influence the cellular generation of ROS, from sources such as NADPH oxidases and mitochondria. This relationship has been explored in great depth during the process of apoptosis, where surges of Ca2+ and ROS are important mediators of cell death. More recently, coordinated and localized Ca2+ and ROS transients appear to play a major role in a vast variety of pro-survival signaling pathways that may be crucial for both physiological and pathophysiological functions. While much work is required to firmly establish this Ca2+-ROS relationship in cancer, existing evidence from other disease models suggests this crosstalk is likely of significant importance in tumorigenesis. In this review, we describe the regulation of Ca2+ channels and transporters by oxidants and discuss the potential consequences of the ROS-Ca2+ interplay in tumor cells.

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U2 - 10.1016/j.ceca.2017.01.007

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