55
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Targeting calcium signaling in cancer therapy.

      1 , 2 , 3 , 4
      Acta pharmaceutica Sinica. B
      Elsevier BV
      20-GPPD, 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol, Apoptosis, CBD, cannabidiol, CBG, cannabigerol, CPZ, capsazepine, CRAC, Ca2+ release-activated Ca2+ channel, CTL, cytotoxic T cells, CYP3A4, cytochrome P450 3A4, Ca2+ channels, CaM, calmodulin, CaMKII, calmodulin-dependent protein kinase II, Cancer therapy, Cell proliferation, Channel blockers;, 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), 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, Migration, NCX, Na+/Ca2+ exchanger, NF-κB, nuclear factor-κB, NFAT, nuclear factor of activated T cells, 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, Store-operated Ca2+ entry, 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, mAb, monoclonal antibody

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The intracellular calcium ions (Ca2+) act as second messenger to regulate gene transcription, cell proliferation, migration and death. Accumulating evidences have demonstrated that intracellular Ca2+ homeostasis is altered in cancer cells and the alteration is involved in tumor initiation, angiogenesis, progression and metastasis. Targeting derailed Ca2+ signaling for cancer therapy has become an emerging research area. This review summarizes some important Ca2+ channels, transporters and Ca2+-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 Ca2+ channels/transporters or Ca2+-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 Ca2+ signaling in different cancer cells, and to search for novel therapies to cure these malignancies by targeting Ca2+ channels or transporters.

          Related collections

          Most cited references188

          • Record: found
          • Abstract: found
          • Article: not found

          Calcium oscillations increase the efficiency and specificity of gene expression.

          Cytosolic calcium ([Ca2+]i) oscillations are a nearly universal mode of signalling in excitable and non-excitable cells. Although Ca2+ is known to mediate a diverse array of cell functions, it is not known whether oscillations contribute to the efficiency or specificity of signalling or are merely an inevitable consequence of the feedback control of [Ca2+]i. We have developed a Ca2+ clamp technique to investigate the roles of oscillation amplitude and frequency in regulating gene expression driven by the proinflammatory transcription factors NF-AT, Oct/OAP and NF-kappaB. Here we report that oscillations reduce the effective Ca2+ threshold for activating transcription factors, thereby increasing signal detection at low levels of stimulation. In addition, specificity is encoded by the oscillation frequency: rapid oscillations stimulate all three transcription factors, whereas infrequent oscillations activate only NF-kappaB. The genes encoding the cytokines interleukin (IL)-2 and IL-8 are also frequency-sensitive in a way that reflects their degree of dependence on NF-AT versus NF-kappaB. Our results provide direct evidence that [Ca2+]i oscillations increase both the efficacy and the information content of Ca2+ signals that lead to gene expression and cell differentiation.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Imaging interorganelle contacts and local calcium dynamics at the ER-mitochondrial interface.

            The ER-mitochondrial junction provides a local calcium signaling domain that is critical for both matching energy production with demand and the control of apoptosis. Here, we visualize ER-mitochondrial contact sites and monitor the localized [Ca(2+)] changes ([Ca(2+)](ER-mt)) using drug-inducible fluorescent interorganelle linkers. We show that all mitochondria have contacts with the ER, but plasma membrane (PM)-mitochondrial contacts are less frequent because of interleaving ER stacks in both RBL-2H3 and H9c2 cells. Single mitochondria display discrete patches of ER contacts and show heterogeneity in the ER-mitochondrial Ca(2+) transfer. Pericam-tagged linkers revealed IP(3)-induced [Ca(2+)](ER-mt) signals that exceeded 9 microM and endured buffering bulk cytoplasmic [Ca(2+)] increases. Altering linker length to modify the space available for the Ca(2+) transfer machinery had a biphasic effect on [Ca(2+)](ER-mt) signals. These studies provide direct evidence for the existence of high-Ca(2+) microdomains between the ER and mitochondria and suggest an optimal gap width for efficient Ca(2+) transfer. 2010 Elsevier Inc. All rights reserved.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Orai1 and STIM1 are critical for breast tumor cell migration and metastasis.

              Tumor metastasis is the primary cause of death of cancer patients. Understanding the molecular mechanisms underlying tumor metastasis will provide potential drug targets. We report here that Orai1 and STIM1, both of which are involved in store-operated calcium entry, are essential for breast tumor cell migration in vitro and tumor metastasis in mice. Reduction of Orai1 or STIM1 by RNA interference in highly metastatic human breast cancer cells or treatment with a pharmacological inhibitor of store-operated calcium channels decreased tumor metastasis in animal models. Our data demonstrate a role for Orai1 and STIM1 in tumor metastasis and suggest store-operated calcium entry channels as potential cancer therapeutic targets.
                Bookmark

                Author and article information

                Journal
                Acta Pharm Sin B
                Acta pharmaceutica Sinica. B
                Elsevier BV
                2211-3835
                2211-3835
                Jan 2017
                : 7
                : 1
                Affiliations
                [1 ] State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, China; Department of Surgery, Division of Thoracic Surgery, The Ohio State University, Columbus, OH 43210, USA.
                [2 ] Department of Surgery, Division of Thoracic Surgery, The Ohio State University, Columbus, OH 43210, USA; Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA.
                [3 ] State Key Laboratory of Oncology in South China; Collaborative Innovation Center for Cancer Medicine, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.
                [4 ] Department of Surgery, Division of Thoracic Surgery, The Ohio State University, Columbus, OH 43210, USA; Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA; College of Nursing and Health Innovation, The University of Texas at Arlington, Arlington, TX 76019, USA.
                Article
                S2211-3835(16)30175-7
                10.1016/j.apsb.2016.11.001
                5237760
                28119804
                e37decc9-86fd-445c-9e73-6e44455bcdd1
                History

                20-GPPD, 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol,Apoptosis,CBD, cannabidiol,CBG, cannabigerol,CPZ, capsazepine,CRAC, Ca2+ release-activated Ca2+ channel,CTL, cytotoxic T cells,CYP3A4, cytochrome P450 3A4,Ca2+ channels,CaM, calmodulin,CaMKII, calmodulin-dependent protein kinase II,Cancer therapy,Cell proliferation,Channel blockers;,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),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,Migration,NCX, Na+/Ca2+ exchanger,NF-κB, nuclear factor-κB,NFAT, nuclear factor of activated T cells,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,Store-operated Ca2+ entry,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,mAb, monoclonal antibody
                20-GPPD, 20-O-β-D-glucopyranosyl-20(S)-protopanaxadiol, Apoptosis, CBD, cannabidiol, CBG, cannabigerol, CPZ, capsazepine, CRAC, Ca2+ release-activated Ca2+ channel, CTL, cytotoxic T cells, CYP3A4, cytochrome P450 3A4, Ca2+ channels, CaM, calmodulin, CaMKII, calmodulin-dependent protein kinase II, Cancer therapy, Cell proliferation, Channel blockers;, 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), 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, Migration, NCX, Na+/Ca2+ exchanger, NF-κB, nuclear factor-κB, NFAT, nuclear factor of activated T cells, 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, Store-operated Ca2+ entry, 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, mAb, monoclonal antibody

                Comments

                Comment on this article