299 results found
Bugan I, Kucuk S, Karagoz Z, et al., 2019, Anti-metastatic effect of ranolazine in an in vivo rat model of prostate cancer, and expression of voltage-gated sodium channel protein in human prostate, PROSTATE CANCER AND PROSTATIC DISEASES, Vol: 22, Pages: 569-579, ISSN: 1365-7852
Djamgoz MBA, Fraser SP, Brackenbury WJ, 2019, In Vivo Evidence for Voltage-Gated Sodium Channel Expression in Carcinomas and Potentiation of Metastasis., Cancers (Basel), Vol: 11, ISSN: 2072-6694
A wide body of evidence suggests that voltage-gated sodium channels (VGSCs) are expressed de novo in several human carcinomas where channel activity promotes a variety of cellular behaviours integral to the metastatic cascade. These include directional motility (including galvanotaxis), pH balance, extracellular proteolysis, and invasion. Contrary to the substantial in vitro data, however, evidence for VGSC involvement in the cancer process in vivo is limited. Here, we critically assess, for the first time, the available in vivo evidence, hierarchically from mRNA level to emerging clinical aspects, including protein-level studies, electrolyte content, animal tests, and clinical imaging. The evidence strongly suggests that different VGSC subtypes (mainly Nav1.5 and Nav1.7) are expressed de novo in human carcinoma tissues and generally parallel the situation in vitro. Consistent with this, tissue electrolyte (sodium) levels, quantified by clinical imaging, are significantly higher in cancer vs. matched non-cancer tissues. These are early events in the acquisition of metastatic potential by the cancer cells. Taken together, the multi-faceted evidence suggests that the VGSC expression has clinical (diagnostic and therapeutic) potential as a prognostic marker, as well as an anti-metastatic target. The distinct advantages offered by the VGSC include especially (1) its embryonic nature, demonstrated most clearly for the predominant neonatal Nav1.5 expression in breast and colon cancer, and (2) the specifically druggable persistent current that VGSCs develop under hypoxic conditions, as in growing tumours, which promotes invasiveness and metastasis.
Farooqi AA, de la Roche M, Djamgoz MBA, et al., 2019, Overview of the oncogenic signaling pathways in colorectal cancer: Mechanistic insights, SEMINARS IN CANCER BIOLOGY, Vol: 58, Pages: 65-79, ISSN: 1044-579X
Guzel RM, Ogmen K, Ilieva KM, et al., 2019, Colorectal cancer invasiveness in vitro: Predominant contribution of neonatal Nav1.5 under normoxia and hypoxia, JOURNAL OF CELLULAR PHYSIOLOGY, Vol: 234, Pages: 6582-6593, ISSN: 0021-9541
Rizaner N, Onkal R, Fraser SP, et al., 2018, Involvement of Intracellular Ca2+Stores in Spontaneous Ca2+Oscillations in a Human Strongly Metastatic Prostate Cancer Cell, Publisher: WILEY, Pages: 52-52, ISSN: 1748-1708
Vysokov NV, Silva J-P, Lelianova VG, et al., 2018, Proteolytically released Lasso/teneurin-2 induces axonal attraction by interacting with latrophilin-1 on axonal growth cones, ELIFE, Vol: 7, ISSN: 2050-084X
Marshall HT, Djamgoz MBA, 2018, Immuno-Oncology: Emerging Targets and Combination Therapies, FRONTIERS IN ONCOLOGY, Vol: 8, ISSN: 2234-943X
Keles D, Sipahi M, Djamgoz MB, et al., 2018, Tetracaine suppress metastatic cell behaviors through regulating matrix metalloproteinase-2/-9 and TIMP-2 levels in metastatic breast cancer cells, Publisher: WILEY, Pages: 334-334, ISSN: 2211-5463
Cort A, Ozben T, Djamgoz MBA, 2018, Oxidative stress and voltage-gated sodium channel activity in human breast cancer cells, Publisher: WILEY, Pages: 359-360, ISSN: 2211-5463
Sipahi M, Keles D, Djamgoz MB, et al., 2018, siRNA-directed inhibition of SCN5A increases matrix metalloproteinase-9 expression and activity in MDA-MB-231 metastatic breast cancer cells, Publisher: WILEY, Pages: 334-334, ISSN: 2211-5463
Pchelintseva E, Djamgoz MBA, 2018, Mesenchymal stem cell differentiation: Control by calcium-activated potassium channels, JOURNAL OF CELLULAR PHYSIOLOGY, Vol: 233, Pages: 3755-3768, ISSN: 0021-9541
Lee A, Djamgoz MBA, 2018, Triple negative breast cancer: Emerging therapeutic modalities and novel combination therapies, CANCER TREATMENT REVIEWS, Vol: 62, Pages: 110-122, ISSN: 0305-7372
Djamgoz MBA, Akun E, Arslan B, et al., 2017, Cancer in North Cyprus: 1. Current Status, An Overview, CYPRUS JOURNAL OF MEDICAL SCIENCES, Vol: 2, Pages: 9-12, ISSN: 2149-7893
Djamgoz MBA, Akun E, Arslan B, et al., 2017, Cancer in North Cyprus: 2. Biomedical Research Activities, CYPRUS JOURNAL OF MEDICAL SCIENCES, Vol: 2, Pages: 13-18, ISSN: 2149-7893
Yamaci RF, Fraser SP, Battaloglu E, et al., 2017, Neonatal Nav1.5 protein expression in normal adult human tissues and breast cancer, PATHOLOGY RESEARCH AND PRACTICE, Vol: 213, Pages: 900-907, ISSN: 0344-0338
Arslan B, Djamgoz MBA, Akün E, 2016, ARSENIC: A Review on Exposure Pathways, Accumulation, Mobility and Transmission into the Human Food Chain., Rev Environ Contam Toxicol, Vol: 243, Pages: 27-51, ISSN: 0179-5953
This review deals with exposure pathways of arsenic (As), as well as its transfer and uptake processes from its source to the human body. It is proven fact that uptake of inorganic As for a long period can lead to chronic As poisoning and a variety of adverse health effects such as skin, lung and bladder cancer, in addition to cardiovascular diseases, diabetes and gastrointestinal symptoms. As exposure occurs primarily from consumption of potable water containing high amounts of inorganic As and also from consumption of crops cultivated in As contaminated agricultural fields-either naturally or anthropogenically through contaminated air or pesticides-or irrigated with As containing water. In this review, light is shed on the transfer mechanism of As through the food chain and the parameters that enhance mobility of As in the environment. Amounts of As accumulation in plants and the transfer mechanisms are also quite different. These differences in As accumulation, such as in leaves, stems, fruits and roots, are discussed in detail. Moreover, presence of As in some vegetables consumed is given by investigating recent research articles that deal with As concentrations, especially in edible parts. Some comparative data are also presented, concerning the level of concentration of As in rice during washing, cooking and processing stages.
Bonito B, Sauter DRP, Schwab A, et al., 2016, K(Ca)3.1 (IK) modulates pancreatic cancer cell migration, invasion and proliferation: anomalous effects on TRAM-34, PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, Vol: 468, Pages: 1865-1875, ISSN: 0031-6768
Rizaner N, Onkal R, Fraser SP, et al., 2016, Intracellular calcium oscillations in strongly metastatic human breast and prostate cancer cells: control by voltage-gated sodium channel activity., European Biophysics Journal, Vol: 45, Pages: 735-748, ISSN: 0175-7571
The possible association of intracellular Ca(2+) with metastasis in human cancer cells is poorly understood. We have studied Ca(2+) signaling in human prostate and breast cancer cell lines of strongly versus weakly metastatic potential in a comparative approach. Intracellular free Ca(2+) was measured using a membrane-permeant fluorescent Ca(2+)-indicator dye (Fluo-4 AM) and confocal microscopy. Spontaneous Ca(2+) oscillations were observed in a proportion of strongly metastatic human prostate and breast cancer cells (PC-3M and MDA-MB-231, respectively). In contrast, no such oscillations were observed in weakly/non metastatic LNCaP and MCF-7 cells, although a rise in the resting Ca(2+) level could be induced by applying a high-K(+) solution. Various parameters of the oscillations depended on extracellular Ca(2+) and voltage-gated Na(+) channel activity. Treatment with either tetrodotoxin (a general blocker of voltage-gated Na(+) channels) or ranolazine (a blocker of the persistent component of the channel current) suppressed the Ca(2+) oscillations. It is concluded that the functional voltage-gated Na(+) channel expression in strongly metastatic cancer cells makes a significant contribution to generation of oscillatory intracellular Ca(2+) activity. Possible mechanisms and consequences of the Ca(2+) oscillations are discussed.
Batcioglu K, Yildirim B, Satilmis B, et al., 2016, Hepatic Arginase - Nitric oxide imbalance: Impact of carcinogenesis and therapeutic effect of sodium channel blockage in an in vivo rat model, TURKISH JOURNAL OF BIOCHEMISTRY-TURK BIYOKIMYA DERGISI, Vol: 41, Pages: 275-279, ISSN: 0250-4685
Vysokov NV, Silva J-P, Lelianova VG, et al., 2016, The Mechanism of Regulated Release of Lasso/Teneurin-2, Frontiers in Molecular Neuroscience, Vol: 9, ISSN: 1662-5099
Teneurins are large cell-surface receptors involved in axon guidance. Teneurin-2 (also known as latrophilin-1-associated synaptic surface organizer (Lasso)) interacts across the synaptic cleft with presynaptic latrophilin-1, an adhesion G-protein-coupled receptor that participates in regulating neurotransmitter release. Lasso-latrophilin-1 interaction mediates synapse formation and calcium signaling, highlighting the important role of this trans-synaptic receptor pair. However, Lasso is thought to be proteolytically cleaved within its ectodomain and released into the medium, making it unclear whether it acts as a proper cell-surface receptor or a soluble protein. We demonstrate here that during its intracellular processing Lasso is constitutively cleaved at a furin site within its ectodomain. The cleaved fragment, which encompasses almost the entire ectodomain of Lasso, is potentially soluble; however, it remains anchored on the cell surface via its non-covalent interaction with the transmembrane fragment of Lasso. Lasso is also constitutively cleaved within the intracellular domain (ICD). Finally, Lasso can be further proteolytically cleaved within the transmembrane domain. The third cleavage is regulated and releases the entire ectodomain of Lasso into the medium. The released ectodomain of Lasso retains its functional properties and binds latrophilin-1 expressed on other cells; this binding stimulates intracellular Ca2+ signaling in the target cells. Thus, Lasso not only serves as a bona fide cell-surface receptor, but also as a partially released target-derived signaling factor.
Djamgoz MB, Pardo LA, 2016, Ion channels, transporters and cancer ("INCA2015"): an international meeting in honor of Prof. Dr. Walter Stühmer., European Biophysics Journal, ISSN: 0175-7571
Aydar E, Stratton D, Fraser SP, et al., 2016, Sigma-1 receptors modulate neonatal Nav1.5 ion channels in breast cancer cell lines., European Biophysics Journal, ISSN: 0175-7571
The main aim of this study was to investigate a possible functional connection between sigma-1 receptors and voltage-gated sodium channels (VGSCs) in human breast cancer cells. The hypothesis was that sigma-1 drugs could alter the metastatic properties of breast cancer cells via the VGSC. Evidence was found for expression of sigma-1 receptor and neonatal Nav1.5 (nNav1.5) expression in both MDA-MB-231 and MDA-MB-468 cells. Sigma-1 drugs (SKF10047 and dimethyltryptamine) did not affect cell proliferation or migration but significantly reduced adhesion to the substrate. Silencing sigma-1 receptor expression by siRNA similarly reduced the adhesion. Blocking nNav1.5 activity with a polyclonal antibody (NESOpAb) targeting an extracellular region of nNav1.5 also reduced the adhesion in both cell lines. Importantly, the results of combined treatments with NESOpAb and a sigma-1 drug or sigma-1 siRNA suggested that both treatments targeted the same mechanism. The possibility was tested, therefore, that the sigma-1 receptor and the nNav1.5 channel formed a physical, functional complex. This suggestion was supported by the results of co-immunoprecipitation experiments. Furthermore, application of sigma-1 drugs to the cells reduced the surface expression of nNav1.5 protein, which could explain how sigma-1 receptor activation could alter the metastatic behaviour of breast cancer cells. Overall, these results are consistent with the idea of a sigma-1 protein behaving like either a "chaperone" or a regulatory subunit associated with nNav1.5.
Bugan I, Karagoz Z, Altun S, et al., 2016, Gabapentin, an Analgesic Used Against Cancer-Associated Neuropathic Pain: Effects on Prostate Cancer Progression in an In Vivo Rat Model, BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY, Vol: 118, Pages: 200-207, ISSN: 1742-7835
Fraser SP, Hemsley F, Djamgoz MBA, 2016, Caffeic acid phenethyl ester: Inhibition of metastatic cell behaviours via voltage-gated sodium channel in human breast cancer in vitro, INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, Vol: 71, Pages: 111-118, ISSN: 1357-2725
Djamgoz MBA, 2015, Blood pressure and risk of cancer progression - A possible connection with salt and voltage-gated sodium channel, MEDICAL HYPOTHESES, Vol: 85, Pages: 591-593, ISSN: 0306-9877
Fraser SP, Foo I, Djamgoz MBA, 2015, Local anaesthetic use in cancer surgery and disease recurrence: role of voltage-gated sodium channels? (vol 113, pg 899, 2015), BRITISH JOURNAL OF ANAESTHESIA, Vol: 114, Pages: 1014-1014, ISSN: 0007-0912
Fraser SP, Foo I, Djamgoz MBA, 2014, Local anaesthetic use in cancer surgery and disease recurrence: role of voltage-gated sodium channels?, BRITISH JOURNAL OF ANAESTHESIA, Vol: 113, Pages: 899-902, ISSN: 0007-0912
Fraser SP, Ozerlat-Gunduz I, Brackenbury WJ, et al., 2014, Regulation of voltage-gated sodium channel expression in cancer: hormones, growth factors and auto-regulation, PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, Vol: 369, ISSN: 0962-8436
Djamgoz MBA, Coombes RC, Schwab A, 2014, Ion transport and cancer: from initiation to metastasis Introduction, PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, Vol: 369, ISSN: 0962-8436
Fraser SP, Peters A, Fleming-Jones S, et al., 2014, Resveratrol: Inhibitory Effects on Metastatic Cell Behaviors and Voltage-Gated Na+ Channel Activity in Rat Prostate Cancer In Vitro, NUTRITION AND CANCER-AN INTERNATIONAL JOURNAL, Vol: 66, Pages: 1047-1058, ISSN: 0163-5581
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