Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28143649&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Crosstalk between calcium and reactive oxygen species signaling in cancer #MMPMID28143649
Hempel N; Trebak M
Cell Calcium 2017[May]; 63 (?): 70-96 PMID28143649show ga
The interplay between Ca(2+) and reactive oxygen species (ROS) signaling pathways is well established, with reciprocal regulation occurring at a number of subcellular locations. Many Ca(2+) channels at the cell surface and intracellular organelles, including the endoplasmic reticulum and mitochondria are regulated by redox modifications. In turn, Ca(2+) 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 Ca(2+) and ROS are important mediators of cell death. More recently, coordinated and localized Ca(2+) 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 Ca(2+)-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 Ca(2+) channels and transporters by oxidants and discuss the potential consequences of the ROS-Ca(2+) interplay in tumor cells.
free
free
free
Cell+Calcium 2017 ; 63 (?): 70-96
