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| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| Normal Healthy |
| 2601- | Ba, | Cardioprotective effects of baicalein on heart failure via modulation of Ca2 + handling proteins in vivo and in vitro |
| - | in-vitro, | Nor, | NA | - | in-vivo, | Nor, | NA |
| 2689- | BBR, | Berberine protects against glutamate-induced oxidative stress and apoptosis in PC12 and N2a cells |
| - | in-vitro, | Nor, | PC12 | - | in-vitro, | AD, | NA | - | in-vitro, | Stroke, | NA |
| 2684- | BBR, | Berberine is a Novel Mitochondrial Calcium Uniporter Inhibitor that Disrupts MCU‐EMRE Assembly |
| - | in-vivo, | Nor, | NA |
| 1585- | Citrate, | Sodium citrate targeting Ca2+/CAMKK2 pathway exhibits anti-tumor activity through inducing apoptosis and ferroptosis in ovarian cancer |
| - | in-vitro, | Ovarian, | SKOV3 | - | in-vitro, | Ovarian, | A2780S | - | in-vitro, | Nor, | HEK293 |
| 1974- | EGCG, | Protective Effect of Epigallocatechin-3-Gallate in Hydrogen Peroxide-Induced Oxidative Damage in Chicken Lymphocytes |
| - | in-vitro, | Nor, | NA |
| 2468- | EGCG, | Green tea epigallocatechin-3-gallate inhibits platelet signalling pathways triggered by both proteolytic and non-proteolytic agonists |
| - | in-vitro, | Nor, | NA |
| 2236- | MF, | Changes in Ca2+ release in human red blood cells under pulsed magnetic field |
| - | in-vitro, | Nor, | NA |
| 2237- | MF, | The Effect of Pulsed Electromagnetic Field Stimulation of Live Cells on Intracellular Ca2+ Dynamics Changes Notably Involving Ion Channels |
| - | in-vitro, | AML, | KG-1 | - | in-vitro, | Nor, | HUVECs |
| 2261- | MF, | Tumor-specific inhibition with magnetic field |
| - | in-vitro, | Nor, | GP-293 | - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Lung, | A549 |
| 507- | MF, | Effects of extremely low frequency electromagnetic fields on the tumor cell inhibition and the possible mechanism |
| - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Lung, | A549 | - | in-vitro, | Nor, | GP-293 |
| 2006- | PLB, | Plumbagin induces apoptosis in human osteosarcoma through ROS generation, endoplasmic reticulum stress and mitochondrial apoptosis pathway |
| - | in-vitro, | OS, | MG63 | - | in-vitro, | Nor, | hFOB1.19 |
| 3342- | QC, | Quercetin modulates OTA-induced oxidative stress and redox signalling in HepG2 cells — up regulation of Nrf2 expression and down regulation of NF-κB and COX-2 |
| - | in-vitro, | Nor, | HepG2 |
| 2467- | RES, | Resveratrol inhibits Ca2+ signals and aggregation of platelets |
| - | in-vitro, | Nor, | NA |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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