%0 Journal Article
%T Cancer-Associated Intermediate Conductance Ca2+-Activated K+ Channel KCa3.1
%A Corinna J. Mohr
%A Dominic Gross
%A Friederike A. Steudel
%A Hiltrud Brauch
%A Peter Ruth
%A Reiner Hoppe
%A Robert Lukowski
%A Stephan M. Huber
%A Werner Schroth
%A Wing-Yee Lo
%J Archive of "Cancers".
%D 2019
%R 10.3390/cancers11010109
%X Several tumor entities have been reported to overexpress KCa3.1 potassium channels due to epigenetic, transcriptional, or post-translational modifications. By modulating membrane potential, cell volume, or Ca2+ signaling, KCa3.1 has been proposed to exert pivotal oncogenic functions in tumorigenesis, malignant progression, metastasis, and therapy resistance. Moreover, KCa3.1 is expressed by tumor-promoting stroma cells such as fibroblasts and the tumor vasculature suggesting a role of KCa3.1 in the adaptation of the tumor microenvironment. Combined, this features KCa3.1 as a candidate target for innovative anti-cancer therapy. However, immune cells also express KCa3.1 thereby contributing to T cell activation. Thus, any strategy targeting KCa3.1 in anti-cancer therapy may also modulate anti-tumor immune activity and/or immunosuppression. The present review article highlights the potential of KCa3.1 as an anti-tumor target providing an overview of the current knowledge on its function in tumor pathogenesis with emphasis on vasculo- and angiogenesis as well as anti-cancer immune responses
%K KCa3.1
%K intermediate conductance calcium-activated K+ channel
%K BK
%K big conductance Ca2+- and voltage-activated K+ channels
%K TRAM-34
%K (1-[(2-chlorophenyl) diphenylmethyl]-pyrazole
%K 1-EBIO
%K 1-Ethyl-1
%K 3-dihydro-2H-benzimidazol-2-one
%K E2
%K 17¦Â-estradiol
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6357066/