13 December 2016
20-GPPD, 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol, CaM, calmodulin, CaMKII, calmodulin-dependent protein kinase II, CBD, cannabidiol, CBG, cannabigerol, CPZ, capsazepine, CRAC, Ca2+ release-activated Ca2+ channel, CTL, cytotoxic T cells, CYP3A4, cytochrome P450 3A4, ER/SR, endoplasmic/sarcoplasmic reticulum, HCX, H+/Ca2+ exchangers, IP3, inositol 1,4,5-trisphosphate, IP3R (1, 2, 3), IP3 receptor (type 1, type 2, type 3), mAb, monoclonal antibody, MCU, mitochondrial Ca2+ uniporter, MCUR1, MCU uniporter regulator 1, MICU (1, 2, 3), mitochondrial calcium uptake (type 1, type 2, type 3), MLCK, myosin light-chain kinase, NCX, Na+/Ca2+ exchanger, NFAT, nuclear factor of activated T cells, NF-κB, nuclear factor-κB, NSCLC, non-small cell lung cancer, OSCC, oral squamous cell carcinoma cells, PKC, protein kinase C, PM, plasma membrane, PMCA, plasma membrane Ca2+-ATPase, PTP, permeability transition pore, ROS, reactive oxygen species, RyR, ryanodine receptor, SERCA, SR/ER Ca2+-ATPase, SOCE, store-operated Ca2+ entry, SPCA, secretory pathway Ca2+-ATPase, TEA, tetraethylammonium, TG, thapsigargin, TPC2, two-pore channel 2, TRIM, 1-(2-(trifluoromethyl) phenyl) imidazole, TRP (A, C, M, ML, N, P, V), transient receptor potential (ankyrin, canonical, melastatin, mucolipin, no mechanoreceptor potential C, polycystic, vanilloid) , VGCC, voltage-gated Ca2+ channel, Ca2+ channels, Store-operated Ca2+ entry, Cell proliferation, Migration, Apoptosis, Channel blockers;, Cancer therapy
The intracellular calcium ions (Ca 2+) act as second messenger to regulate gene transcription, cell proliferation, migration and death. Accumulating evidences have demonstrated that intracellular Ca 2+ homeostasis is altered in cancer cells and the alteration is involved in tumor initiation, angiogenesis, progression and metastasis. Targeting derailed Ca 2+ signaling for cancer therapy has become an emerging research area. This review summarizes some important Ca 2+ channels, transporters and Ca 2+-ATPases, which have been reported to be altered in human cancer patients. It discusses the current research effort toward evaluation of the blockers, inhibitors or regulators for Ca 2+ channels/transporters or Ca 2+-ATPase pumps as anti-cancer drugs. This review is also aimed to stimulate interest in, and support for research into the understanding of cellular mechanisms underlying the regulation of Ca 2+ signaling in different cancer cells, and to search for novel therapies to cure these malignancies by targeting Ca 2+ channels or transporters.
Ca 2+ plays vital roles in normal cell physiology, such as gene transcription, cell proliferation and migration. Abnormal Ca 2+ signaling by virtue of altered channel expression or activation contributes to carcinogenesis and promotes tumor development. Targeting the dysregulated Ca 2+ channels/transporters/pumps may provide a promising chemotherapy for cancer treatment.