TY - JOUR
T1 - Crosstalk between calcium and reactive oxygen species signaling in cancer
AU - Hempel, Nadine
AU - Trebak, Mohamed
N1 - Funding Information:
Research in the authors’ laboratories are funded by grants R01HL123364, R01HL097111, R21AG050072 from the NIH, grant NPRP8-110-3-021 from the Qatar National Research Fund (GNRF) and grant 14GRNT18880008 from the AHA to MT, and by grant W81XWH-16-1-0117 from the Department of Defense (DoD) to NH. The authors have no conflict of interests to declare.
Publisher Copyright:
© 2017 Elsevier Ltd
PY - 2017/5
Y1 - 2017/5
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.
UR - http://www.scopus.com/inward/record.url?scp=85010976723&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85010976723&partnerID=8YFLogxK
U2 - 10.1016/j.ceca.2017.01.007
DO - 10.1016/j.ceca.2017.01.007
M3 - Review article
C2 - 28143649
AN - SCOPUS:85010976723
SN - 0143-4160
VL - 63
SP - 70
EP - 96
JO - Cell Calcium
JF - Cell Calcium
ER -