How Dysregulated Ion Channels and Transporters Take a Hand in Esophageal, Liver, and Colorectal Cancer
Over the last two decades, the understanding of how dysregulated ion channels and transporters are involved in carcinogenesis and tumor growth and progression, including invasiveness and metastasis, has been increasing exponentially. The present review sp
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How Dysregulated Ion Channels and Transporters Take a Hand in Esophageal, Liver, and Colorectal Cancer Christian Stock
Contents 1 Introduction 1.1 Risk Factors Dysregulating Ion Channels and Transporters 2 Esophageal Cancer 2.1 Ca2+ Channels and Transporters 2.2 Transient Receptor Potential (TRP) Channels 2.3 K+ Channels 2.4 Cl Channels 2.5 Na+/H+ Exchanger 1 (SLC9A1) 2.6 Divalent Metal Transporter 3 Hepatocellular Carcinoma 3.1 Ca2+ Channels and Transporters 3.2 Transient Receptor Potential (TRP) Channels 3.3 K+ Channels 3.4 Na+ Channels 3.5 Cl Channels 3.6 Na+/H+ Exchanger NHE1 (SLC9A1) 3.7 Monocarboxylate Transporters (MCTs, SLC16As) 3.8 Magnesium Transporter MagT1 3.9 Organic Anion and Cation Transporters 4 Colorectal Cancer 4.1 Ca2+ Channels and Transporters 4.2 Transient Receptor Potential (TRP) Channels 4.3 K+ Channels 4.4 Na+ Channels 4.5 Cl Channels 4.6 Na+/H+ Exchangers 4.7 NBC (SLC4A4, NBCe1) 4.8 Cl/HCO3 Exchanger (DRA, SLC26A3) 4.9 Monocarboxylate Carriers (MCTs, SLC16As) 4.10 SO42 Transporter (SLC26A2, DTDST) 4.11 Zn2+ Transporters
C. Stock (*) Department of Gastroenterology, Hannover Medical School, Hannover, Germany e-mail: [email protected]
C. Stock 4.12 Organic Cation Transporters 4.13 Organic Anion Transporters 5 Conclusion References
Abstract Over the last two decades, the understanding of how dysregulated ion channels and transporters are involved in carcinogenesis and tumor growth and progression, including invasiveness and metastasis, has been increasing exponentially. The present review specifies virtually all ion channels and transporters whose faulty expression or regulation contributes to esophageal, hepatocellular, and colorectal cancer. The variety reaches from Ca2+, K+, Na+, and Cl channels over divalent metal transporters, Na+ or Cl coupled Ca2+, HCO3 and H+ exchangers to monocarboxylate carriers and organic anion and cation transporters. In several cases, the underlying mechanisms by which these ion channels/transporters are interwoven with malignancies have been fully or at least partially unveiled. Ca2+, Akt/NF-κB, and Ca2+- or pH-dependent Wnt/β-catenin signaling emerge as cross points through which ion channels/transporters interfere with gene expression, modulate cell proliferation, trigger epithelial-to-mesenchymal transition, and promote cell motility and metastasis. Also miRs, lncRNAs, and DNA methylation represent potential links between the misexpression of genes encoding for ion channels/transporters, their malfunctioning, and cancer. The knowledge of all these molecular interactions has provided the basis for therapeutic strategies and approaches, some of which will be broached in this review. Keywords Akt/NF-κB · Ca2+ · Carcinogenesis · Metastasis · pH · Wnt/β-catenin
1 Introduction The activity of ion channels and transporters impacts and, at the same time, depends on (1) a cell’s membrane potential, (2) cell volume, and (3) cellular pH and Ca2+ homeostasis. This interdependence of physiological variables has been thrown off balance in the vast
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