Plasma membrane ion channels and epithelial to mesenchymal transition in cancer cells

  1. Gregory R Monteith1,2,3
  1. 1The School of Pharmacy, The University of Queensland, Brisbane, Queensland, Australia
  2. 2Mater Research Institute, The University of Queensland, Brisbane, Queensland, Australia
  3. 3Translational Research Institute, Brisbane, Queensland, Australia
  1. Correspondence should be addressed to G R Monteith; Email: gregm{at}
  1. Figure 1

    Epithelial to mesenchymal transition (EMT). EMT is a reversible process whereby epithelial cells with polygonal morphology, apical–basal polarity, and high cell–cell/cell–ECM adhesion, and stationary position acquire mesenchymal features including spindle-like morphology, anterior–posterior polarity, cell–cell/cell–ECM dissociation and enhanced motility. EMT can be induced by microenvironmental factors including growth factors, cytokines and hypoxia. The reverse process of EMT is called mesenchymal to epithelial transition (MET).

  2. Figure 2

    Plasma membrane ion channels. Plasma membrane calcium channels include Orai (activated by Ca2+ store depletion), transient receptor potential (TRP), P2X (activated by ligands such as ATP), and voltage gated Ca2+ channels (VGCC). Plasma membrane sodium channels include voltage-gated sodium channels (VGSC), sodium leak channel (NALCN) and epithelial sodium channel (ENaC). Plasma membrane potassium channels include voltage gated channels (VGKC two-pore domain (K2P) channels, Ca2+-activated channels (KCa) and inwardly rectifying channels (IRK). Plasma membrane chloride channels include maxi channels, cystic fibrosis transmembrane conductance regulator (CFTR), Ca2+-activated channels (CaCC), ligand-gated channels (LGCC), volume-regulated anion channels (VRAC), and the chloride channel superfamily (CIC).

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