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Production and Detection of Reactive Oxygen Species ROS in Cancers
Published on: November 21, 2011
Crosstalk between calcium and reactive oxygen species signaling in cancer
Nadine Hempel1, Mohamed Trebak2
1Department of Pharmacology, Penn State College of Medicine, Hershey PA 17033, United States; Penn State Hershey Cancer Institute, Penn State College of Medicine, Hershey PA 17033, United States.
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.
Insights
Calcium (Ca2+) and reactive oxygen species (ROS) signaling pathways are interconnected. This review explores their crosstalk in cancer, highlighting Ca2+ channel regulation by oxidants and implications for tumor cells.
Area of Science:
- Cellular signaling
- Oxidative stress biology
- Cancer research
Background:
- Calcium (Ca2+) and reactive oxygen species (ROS) signaling pathways exhibit reciprocal regulation across various subcellular locations.
- Ca2+ channels in cell surface and intracellular organelles are modulated by redox modifications.
- Ca2+ signaling influences cellular ROS generation from sources like NADPH oxidases and mitochondria.
Purpose of the Study:
- To review the regulation of Ca2+ channels and transporters by oxidants.
- To discuss the potential consequences of ROS-Ca2+ interplay in tumor cells.
- To highlight the significance of this crosstalk in tumorigenesis.
Main Methods:
- Literature review of existing research on Ca2+ and ROS signaling.
- Analysis of studies investigating redox regulation of Ca2+ channels.
- Examination of evidence linking ROS-Ca2+ interplay to cancer and other disease models.
Main Results:
- Ca2+ channels and transporters are demonstrably regulated by oxidants.
- ROS-Ca2+ signaling plays roles in both cell death (apoptosis) and pro-survival pathways.
- Evidence suggests significant importance of this crosstalk in tumorigenesis, though further research is needed.
Conclusions:
- The interplay between Ca2+ and ROS is a critical regulatory mechanism with implications for cellular function.
- Understanding ROS-Ca2+ crosstalk is crucial for elucidating mechanisms of tumorigenesis.
- Targeting this interplay may offer novel therapeutic strategies for cancer.
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