N-Myc-induced up-regulation of TRPM6/TRPM7 channels promotes neuroblastoma cell proliferation

Zhang, Zheng; Faouzi, Malika; Huang, Junhao; Geerts, Dirk; Hou, Yu; Fleig, Andrea; Penner, Reinhold

doi:10.18632/oncotarget.2283

Cited by 31 publications

(26 citation statements)

References 41 publications

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“…Moreover, TRPM7 silencing also decreases MCF-7 proliferation in a Ca 2+ -dependent manner. Similar results were found in retinoblastoma (Hanano et al 2004), in head and neck squamous carcinoma (Jiang et al 2007) and in neuroblastoma (Zhang et al 2014) cell lines suggesting that TRPM7 channels promote constitutive Ca 2+ uptake and regulate basal intracellular Ca 2+ levels leading to sustained proliferation of cancer cells.…”

Section: Trpm7 Is Involved In Cancer Cell Fates Through Different Mecsupporting

confidence: 79%

Constitutive calcium entry and cancer: updated views and insights

et al. 2017

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Tight control of basal cytosolic Ca concentration is essential for cell survival and to fine-tune Ca-dependent cell functions. A way to control this basal cytosolic Ca concentration is to regulate membrane Ca channels including store-operated Ca channels and secondary messenger-operated channels linked to G-protein-coupled or tyrosine kinase receptor activation. Orai, with or without its reticular STIM partner and Transient Receptor Potential (TRP) proteins, were considered to be the main Ca channels involved. It is well accepted that, in response to cell stimulation, opening of these Ca channels contributes to Ca entry and the transient increase in cytosolic Ca concentration involved in intracellular signaling. However, in various experimental conditions, Ca entry and/or Ca currents can be recorded at rest, without application of any experimental stimulation. This led to the proposition that some plasma membrane Ca channels are already open/activated in basal condition, contributing therefore to constitutive Ca entry. This article focuses on direct and indirect observations supporting constitutive activity of channels belonging to the Orai and TRP families and on the mechanisms underlying their basal/constitutive activities.

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Section: Trpm7 Is Involved In Cancer Cell Fates Through Different Mecsupporting

confidence: 79%

Constitutive calcium entry and cancer: updated views and insights

et al. 2017

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“…Several types of Ca 2ϩ entry and Ca 2ϩ release channels have been implicated in such remodeling in various cancer types (FIGURE 2, blue color). Among them are ORAI1 and STIM1 SOC components (78,136,218,260,308,420,558,569); TRP members TRPV6 (44,136,289,290,420), TRPC1, TRPC3, TRPC4 and TRPC6 (15, 19, 85, 117-119, 247, 458, 460, 485, 487, 557), TRPM2 (556), TRPM6/7 (117,190,475,554,560); Ca v family members (58,381,562); as well as IP 3 R (436,481) and RyR (3) ER release channels. Most of the relevant data, however, were obtained by comparing respective channels mRNA expression in normal and cancer tissues and assaying proliferative activity of related cancer cell lines in the in vitro setting in response to pharmacological or siRNA-mediated impairment of channels function and/or expression.…”

Section: Oncogenic Alterations In Ca 2ϩ Signalingmentioning

confidence: 99%

Ion Channels in Cancer: Are Cancer Hallmarks Oncochannelopathies?

Prevarskaya

Skryma

Shuba³

2018

Physiological Reviews

317

292

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Genomic instability is a primary cause and fundamental feature of human cancer. However, all cancer cell genotypes generally translate into several common pathophysiological features, often referred to as cancer hallmarks. Although nowadays the catalog of cancer hallmarks is quite broad, the most common and obvious of them are 1) uncontrolled proliferation, 2) resistance to programmed cell death (apoptosis), 3) tissue invasion and metastasis, and 4) sustained angiogenesis. Among the genes affected by cancer, those encoding ion channels are present. Membrane proteins responsible for signaling within cell and among cells, for coupling of extracellular events with intracellular responses, and for maintaining intracellular ionic homeostasis ion channels contribute to various extents to pathophysiological features of each cancer hallmark. Moreover, tight association of these hallmarks with ion channel dysfunction gives a good reason to classify them as special type of channelopathies, namely oncochannelopathies. Although the relation of cancer hallmarks to ion channel dysfunction differs from classical definition of channelopathies, as disease states causally linked with inherited mutations of ion channel genes that alter channel's biophysical properties, in a broader context of the disease state, to which pathogenesis ion channels essentially contribute, such classification seems absolutely appropriate. In this review the authors provide arguments to substantiate such point of view.

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“…In addition, TRPM6 mutation (p.R1122Q) affecting its topological domain towards the cytoplasm occurs in a small proportion of breast cancer patients , and two other TRPM6 somatic mutations (p.T1822A and p.A1765T) have also been observed in an independent cohort of breast cancer samples (Stephens et al, 2012). heteromer (Zhang et al, 2014a). Such heteromerization leads to further functional diversification and assessment of both TRPM6 and TRPM7 oncogenic properties might also need to consider the presence and relevance of TRPM6/7 heteromers especially when both channels are expressed in the same cancer cells.…”

Section: Trpm5: a Potential Oncochannel In Melanomamentioning

confidence: 99%

The oncogenic roles of TRPM ion channels in cancer

Wong

Banham

Yaacob

et al. 2019

Journal Cellular Physiology

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Transient receptor potential (TRP) proteins are a diverse family of ion channels present in multiple types of tissues. They function as gatekeepers for responses to sensory stimuli including temperature, vision, taste, and pain through their activities in conducting ion fluxes. The TRPM (melastatin) subfamily consists of eight members (i.e., TRPM1–8), which collectively regulate fluxes of various types of cations such as K+, Na+, Ca2+, and Mg2+. Growing evidence in the past two decades indicates that TRPM ion channels, their isoforms, or long noncoding RNAs encoded within the locus may be oncogenes involved in the regulation of cancer cell growth, proliferation, autophagy, invasion, and epithelial–mesenchymal transition, and their significant association with poor clinical outcomes of cancer patients. In this review, we describe and discuss recent findings implicating TRPM channels in different malignancies, their functions, mechanisms, and signaling pathways involved in cancers, as well as summarizing their normal physiological functions and the availability of ion channel pharmacological inhibitors.

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N-Myc-induced up-regulation of TRPM6/TRPM7 channels promotes neuroblastoma cell proliferation

Cited by 31 publications

References 41 publications

Constitutive calcium entry and cancer: updated views and insights

Constitutive calcium entry and cancer: updated views and insights

Ion Channels in Cancer: Are Cancer Hallmarks Oncochannelopathies?

The oncogenic roles of TRPM ion channels in cancer

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