ER Ca2+ release and store-operated Ca2+ entry – partners in crime or independent actors in oncogenic transformation?

Pierro, Cristina; Sneyers, Flore; Bultynck, Geert; Roderick, H. Llewelyn

doi:10.1016/j.ceca.2019.102061

Cited by 19 publications

(22 citation statements)

References 199 publications

(232 reference statements)

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“…1 ) as well as by fine-tuning mechanisms affecting proteins involved in Ca 2+ transport. Thus, Ca 2+ is shuttled between extracellular space, cytosol, ER or SR, mitochondria and, to a lesser extent, to Golgi apparatus and lysosomes [ 44 ].…”

Section: Ca 2+ Homeostasismentioning

confidence: 99%

“…The stromal interaction molecules 1 and 2 (STIM1 and STIM2) sense Ca 2+ concentration within the ER. As soon as ER Ca 2+ levels drop, STIM proteins aggregate and initiate the recruitment and opening of ORAI channels (ORAI1, ORAI2 and ORAI3) in the plasma membranes, which is followed by a rapid Ca 2+ influx [ 44 ]. Ca 2+ from the cytosol is taken up into the ER via the sarco/endoplasmic reticulum ATPase (SERCA) at the expense of ATP.…”

Section: Ca 2+ Homeostasismentioning

confidence: 99%

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Interrelation between ROS and Ca2+ in aging and age-related diseases

2020

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Calcium (Ca 2+ ) and reactive oxygen species (ROS) are versatile signaling molecules coordinating physiological and pathophysiological processes. While channels and pumps shuttle Ca 2+ ions between extracellular space, cytosol and cellular compartments, short-lived and highly reactive ROS are constantly generated by various production sites within the cell. Ca 2+ controls membrane potential, modulates mitochondrial adenosine triphosphate (ATP) production and affects proteins like calcineurin (CaN) or calmodulin (CaM), which, in turn, have a wide area of action. Overwhelming Ca 2+ levels within mitochondria efficiently induce and trigger cell death. In contrast, ROS comprise a diverse group of relatively unstable molecules with an odd number of electrons that abstract electrons from other molecules to gain stability. Depending on the type and produced amount, ROS act either as signaling molecules by affecting target proteins or as harmful oxidative stressors by damaging cellular components. Due to their wide range of actions, it is little wonder that Ca 2+ and ROS signaling pathways overlap and impact one another. Growing evidence suggests a crucial implication of this mutual interplay on the development and enhancement of age-related disorders, including cardiovascular and neurodegenerative diseases as well as cancer.

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Section: Ca 2+ Homeostasismentioning

confidence: 99%

Section: Ca 2+ Homeostasismentioning

confidence: 99%

Interrelation between ROS and Ca2+ in aging and age-related diseases

2020

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“…Changes in the cytosolic Ca 2+ concentration ([Ca 2+ ] c ) due to Ca 2+ entry across the plasma membrane have been reported to be involved in cell proliferation [1][2][3][4]. In fact, several cancer cell lines present altered [Ca 2+ ] c due to dysregulation of Ca 2+ entry mechanisms, among others [3,[5][6][7][8][9]. The Ca 2+ currents I SOC , I CRAC , and I ARC were described as relevant inward Ca 2+ currents in non-excitable cells including several cancer cell types [10,11].…”

Section: Introductionmentioning

confidence: 99%

Arachidonic Acid Attenuates Cell Proliferation, Migration and Viability by a Mechanism Independent on Calcium Entry

Cantonero

Sánchez-Collado

López

et al. 2020

IJMS

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Arachidonic acid (AA) is a phospholipase A2 metabolite that has been reported to mediate a plethora of cellular mechanisms involved in healthy and pathological states such as platelet aggregation, lymphocyte activation, and tissue inflammation. AA has been described to activate Ca2+ entry through the arachidonate-regulated Ca2+-selective channels (ARC channels). Here, the analysis of the changes in the intracellular Ca2+ homeostasis revealed that, despite MDA-MB-231 cells expressing the ARC channel components Orai1, Orai3, and STIM1, AA does not evoke Ca2+ entry in these cells. We observed that AA evokes Ca2+ entry in MDA-MB-231 cells transiently expressing ARC channels. Nevertheless, MDA-MB-231 cell treatment with AA reduces cell proliferation and migration while inducing cell death through apoptosis. The latter mostly likely occurs via mitochondria membrane depolarization and the activation of caspases-3, -8, and -9. Altogether, our results indicate that AA exerts anti-tumoral effects on MDA-MB-231 cells, without having any effect on non-tumoral breast epithelial cells, by a mechanism that is independent on the activation of Ca2+ influx via ARC channels.

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“…For instance, in neurodegenerative and age‐related pathologies, such as Alzheimer’s disease and Parkinson’s disease, several disease‐associated proteins are enriched at MCSs (in particular at endoplasmic reticulum (ER)–mitochondria contacts [3,4]), altering key functions (see below) and contributing to pathogenesis. Other pathologies in which MCS abnormalities have been reported include metabolic dysfunctions, like obesity [5], and cancer [6–8]. In this latter condition, for example, a reduced sensitivity to mitochondrial calcium (Ca 2+ ) overload, linked to altered ER–mitochondria Ca 2+ cross‐talk, underlies the resistance (induced by several oncogenes) of tumor cells to death.…”

Section: Introductionmentioning

confidence: 99%

Better to keep in touch: investigating inter‐organelle cross‐talk

2020

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The strategic importance for cellular organelles of being in contact with each other, exchanging messenger molecules, is nowadays well established. Different inter‐organelle cross‐talk pathways finely regulate multiple physiological cellular mechanisms, and their dysregulation has been found to underlie different pathological conditions. In the last years, a great effort has been made to study such organelle interactions, to understand their functional roles within the cell and the molecules involved in their formation and/or modulation. In this contribution, some examples of organelle cross‐talk and their contributions in regulating physiological processes are presented. Moreover, the pro and cons of the available methods for a proper, reliable investigation of membrane contact sites are described.

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ER Ca2+ release and store-operated Ca2+ entry – partners in crime or independent actors in oncogenic transformation?

Cited by 19 publications

References 199 publications

Interrelation between ROS and Ca2+ in aging and age-related diseases

Interrelation between ROS and Ca2+ in aging and age-related diseases

Arachidonic Acid Attenuates Cell Proliferation, Migration and Viability by a Mechanism Independent on Calcium Entry

Better to keep in touch: investigating inter‐organelle cross‐talk

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