<scp>TRP</scp> channels and <scp>STIM</scp>/<scp>ORAI</scp> proteins: sensors and effectors of cancer and stroma cell migration

Nielsen, Nikoline Juul; Lindemann, Otto; Schwab, Albrecht

doi:10.1111/bph.12721

Cited by 53 publications

(45 citation statements)

References 222 publications

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“…In contrast, it is conceivable that sublethal and localized ROS production, might initiate pro-tumorigenic Ca 2+ signaling via activation of cell surface Ca 2+ channels, such as proliferation [119], and wound healing [86]. In both oxidative stress and redox signaling, the location of cell surface Ca 2+ channels clearly makes these an excellent target for sensing redox changes in the intra and extracellular environment [120]. …”

Section: Redox Regulation Of Cellular Ca2+ Homeostasis At the Plasmentioning

confidence: 99%

“…Many of the stimulatory cues that activate plasma membrane channels are often altered in the tumor microenvironment and it is therefore conceivable that altered activity of plasma membrane associated Ca 2+ channels and pumps is a common phenotype of cancer cells[120]. Moreover, remodeling of ion channel expression and alterations in Ca 2+ signaling by plasma membrane cation channels, including TRPC1, TRPC3, TRPC6, TRPM2, TRPM7, TRPV6, ORAI1 and ORAI3 have been implicated in enhanced proliferation of tumor cells[16, 121].…”

Section: Redox Regulation Of Cellular Ca2+ Homeostasis At the Plasmentioning

confidence: 99%

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Crosstalk between calcium and reactive oxygen species signaling in cancer

2017

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The interplay between Ca2+ and reactive oxygen species (ROS) signaling pathways is well established, with reciprocal regulation occurring at a number of subcellular locations. Many Ca2+ channels at the cell surface and intracellular organelles, including the endoplasmic reticulum and mitochondria are regulated by redox modifications. In turn, Ca2+ signaling can influence the cellular generation of ROS, from sources such as NADPH oxidases and mitochondria. This relationship has been explored in great depth during the process of apoptosis, where surges of Ca2+ and ROS are important mediators of cell death. More recently, coordinated and localized Ca2+ and ROS transients appear to play a major role in a vast variety of pro-survival signaling pathways that may be crucial for both physiological and pathophysiological functions. While much work is required to firmly establish this Ca2+-ROS relationship in cancer, existing evidence from other disease models suggests this crosstalk is likely of significant importance in tumorigenesis. In this review, we describe the regulation of Ca2+ channels and transporters by oxidants and discuss the potential consequences of the ROS-Ca2+ interplay in tumor cells.

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Section: Redox Regulation Of Cellular Ca2+ Homeostasis At the Plasmentioning

confidence: 99%

Section: Redox Regulation Of Cellular Ca2+ Homeostasis At the Plasmentioning

confidence: 99%

Crosstalk between calcium and reactive oxygen species signaling in cancer

2017

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“…[10]). Mammalian TRP proteins assemble as homo-or hetero tetramers and build non-selective Ca 2+ -permeable cation channels (refs.…”

Section: Plasma Membrane Calcium Channels and Transportersmentioning

confidence: 99%

Plasma membrane calcium channels in cancer: Alterations and consequences for cell proliferation and migration

Déliot

Constantin

2015

Biochimica et Biophysica Acta (BBA) - Biomembranes

159

140

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The study of calcium channels in molecular mechanisms of cancer transformation is still a novel area of research. Several studies, mostly conducted on cancer cell lines, however support the idea that a diversity of plasma membrane channels participates in the remodeling of Ca2+ homeostasis, which regulates various cancer hallmarks such as uncontrolled multiplication and increase in migration and invasion abilities. However few is still understood concerning the intracellular signaling cascades mobilized by calcium influx participating to cancer cell behavior. This review intends to gather some of these pathways dependent on plasma membrane calcium channels and described in prostate, breast and lung cancer cell lines. In these cancer cell types, the calcium channels involved in calcium signaling pathways promoting cancer behaviors are mostly non-voltage activated calcium channels and belong to the TRP superfamily (TRPC, TPRPV and TRPM families) and the Orai family. TRP and Orai channels are part of many signaling cascades involving the activation of transmembrane receptors by extracellular ligand from the tumor environment. TRPV can sense changes in the physical and chemical environment of cancer cells and TRPM7 are stretch activated and sensitive to cholesterol. Changes in activation and or expression of plasma-membrane calcium channels affect calcium-dependent signaling processes relevant to tumorigenesis. The studies cited in this review suggest that an increase in plasma membrane calcium channel expression and/or activity sustain an elevated calcium entry (constitutive or under the control of extracellular signals) promoting higher cell proliferation and migration in most cases. A variety of non-voltage-operated calcium channels display change expression and/or activity in a same cancer type and cooperate to the same process relevant to cancer cell behavior, or can be involved in a different sequence of events during the tumorigenesis. This article is part of a Special Issue entitled: Membrane channels and transporters in cancers.

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“…TRP channels influence cancer and stroma cell migration via affecting growth factor and cytokine signaling, cytoskeletal remodeling, and adaptation to tumor microenvironment where oxidative stress and hypoxia occur [18].…”

Section: Introductionmentioning

confidence: 99%

“…Several studies revealed that different TRP channels exhibit their effect on stromal cell migration via PI3K activation which is linked to reorganization of cytoskeleton and ERK signaling which regulates the actomyosin network [18]. Examples include TRPV2-dependent migration of macrophages [24], chemotaxis of monocytes relying on TRPC3 channels [25], TRPM7-dependent polarization and fibroblast migration [26], and TRPC6-dependent chemotaxis of neutrophils [27,28].…”

Section: Introductionmentioning

confidence: 99%

Gene expressions of TRP channels in glioblastoma multiforme and relation with survival

et al. 2015

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Glioblastoma multiforme (GBM) is one of the most lethal forms of cancer in humans, with a median survival of 10 to 12 months. Glioblastoma is highly malignant since the cells are supported by a great number of blood vessels. Although new treatments have been developed by increasing knowledge of molecular nature of the disease, surgical operation remains the standard of care. The TRP (transient receptor potential) superfamily consists of cation-selective channels that have roles in sensory physiology such as thermo- and osmosensation and in several complex diseases such as cancer, cardiovascular, and neuronal diseases. The aim of this study was to investigate the expression levels of TRP channel genes in patients with glioblastoma multiforme and to evaluate the relationship between TRP gene expressions and survival of the patients. Thirty-three patients diagnosed with glioblastoma were enrolled to the study. The expression levels of 21 TRP genes were quantified by using qRT-PCR with dynamic array 48 × 48 chip (BioMark HD System, Fluidigm, South San Francisco, CA, USA). TRPC1, TRPC6, TRPM2, TRPM3, TRPM7, TRPM8, TRPV1, and TRPV2 were found significantly higher in glioblastoma patients. Moreover, there was a significant relationship between the overexpression of TRP genes and the survival of the patients. These results demonstrate for the first time that TRP channels contribute to the progression and survival of the glioblastoma patients.

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TRP channels and STIM/ORAI proteins: sensors and effectors of cancer and stroma cell migration

Cited by 53 publications

References 222 publications

Crosstalk between calcium and reactive oxygen species signaling in cancer

Crosstalk between calcium and reactive oxygen species signaling in cancer

Plasma membrane calcium channels in cancer: Alterations and consequences for cell proliferation and migration

Gene expressions of TRP channels in glioblastoma multiforme and relation with survival

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