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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 |
| 5381- | ART/DHA, | Artemisitene triggers calcium-dependent ferroptosis by disrupting the LSH-EWSR1 interaction in colorectal cancer |
| - | in-vitro, | CRC, | HCT116 | - | in-vitro, | Nor, | NCM460 | - | in-vitro, | CRC, | HT29 | - | in-vitro, | CRC, | HCT8 |
| 2474- | Ba, | Anticancer properties of baicalein: a review |
| - | Review, | Var, | NA | - | in-vitro, | Nor, | BV2 |
| 2732- | BetA, | Chemo, | Betulinic acid chemosensitizes breast cancer by triggering ER stress-mediated apoptosis by directly targeting GRP78 |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Nor, | MCF10 |
| 1421- | Bos, | Coupling of boswellic acid-induced Ca2+ mobilisation and MAPK activation to lipid metabolism and peroxide formation in human leucocytes |
| - | in-vitro, | AML, | HL-60 | - | in-vitro, | Nor, | NA |
| 5858- | CAP, | Capsaicin as a Microbiome Modulator: Metabolic Interactions and Implications for Host Health |
| - | Review, | Nor, | NA | - | Review, | AD, | NA |
| 5880- | CAR, | In vitro and in vivo antitumor potential of carvacrol nanoemulsion against human lung adenocarcinoma A549 cells via mitochondrial mediated apoptosis |
| - | vitro+vivo, | Lung, | A549 | - | in-vitro, | Nor, | BEAS-2B | - | in-vitro, | Lung, | PC9 |
| 5926- | CAR, | An Updated Review of Research into Carvacrol and Its Biological Activities |
| - | Review, | Nor, | NA | - | Review, | AD, | NA | - | Review, | asthmatic, | NA |
| 6108- | Chol, | Trimethylamine-N-Oxide (TMAO) as a Rising-Star Metabolite: Implications for Human Health |
| - | Review, | Nor, | NA | - | Review, | AD, | NA |
| 5530- | EP, | Expression of voltage-gated calcium channels augments cell susceptibility to membrane disruption by nanosecond pulsed electric field |
| - | in-vitro, | Nor, | HEK293 |
| 2841- | FIS, | Fisetin, an Anti-Inflammatory Agent, Overcomes Radioresistance by Activating the PERK-ATF4-CHOP Axis in Liver Cancer |
| - | in-vitro, | Nor, | RAW264.7 | - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Liver, | Hep3B | - | in-vitro, | Liver, | HUH7 |
| 4528- | MAG, | Pharmacology, Toxicity, Bioavailability, and Formulation of Magnolol: An Update |
| - | Review, | 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 |
| 2240- | MF, | Pulsed electromagnetic field induces Ca2+-dependent osteoblastogenesis in C3H10T1/2 mesenchymal cells through the Wnt-Ca2+/Wnt-β-catenin signaling pathway |
| - | in-vitro, | Nor, | C3H10T1/2 |
| 2261- | MF, | Tumor-specific inhibition with magnetic field |
| - | in-vitro, | Nor, | GP-293 | - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Lung, | A549 |
| 526- | MF, | Inhibition of Cancer Cell Growth by Exposure to a Specific Time-Varying Electromagnetic Field Involves T-Type Calcium Channels |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | BC, | MCF-7 | - | in-vitro, | Pca, | HeLa | - | vitro+vivo, | Melanoma, | B16-BL6 | - | in-vitro, | Nor, | HEK293 |
| 534- | MF, | Effect of extremely low frequency electromagnetic field parameters on the proliferation of human breast cancer |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 | - | in-vivo, | Nor, | MCF10 |
| 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 |
| 512- | MF, | Pulsed Electromagnetic Fields (PEMFs) Trigger Cell Death and Senescence in Cancer Cells |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Nor, | FF95 |
| 4355- | MF, | Ambient and supplemental magnetic fields promote myogenesis via a TRPC1-mitochondrial axis: evidence of a magnetic mitohormetic mechanism |
| - | in-vitro, | Nor, | C2C12 |
| 3535- | MFrot, | MF, | Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic Implications |
| - | Review, | Nor, | NA |
| 3499- | MFrot, | MF, | Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegans |
| - | in-vitro, | Nor, | HUVECs |
| 3353- | QC, | Quercetin triggers cell apoptosis-associated ROS-mediated cell death and induces S and G2/M-phase cell cycle arrest in KON oral cancer cells |
| - | in-vitro, | Oral, | KON | - | in-vitro, | Nor, | MRC-5 |
| 885- | RES, | Resveratrol induces intracellular Ca2 + rise via T-type Ca2 + channels in a mesothelioma cell line |
| - | in-vitro, | RCC, | REN | - | in-vitro, | Nor, | MeT5A |
| 2550- | SDT, | Intracellular Delivery and Calcium Transients Generated in Sonoporation Facilitated by Microbubbles |
| - | in-vitro, | Nor, | NA |
| 2007- | SK, | Shikonin Directly Targets Mitochondria and Causes Mitochondrial Dysfunction in Cancer Cells |
| - | in-vitro, | lymphoma, | U937 | - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | SkBr3 | - | in-vitro, | CRC, | HCT116 | - | in-vitro, | OS, | U2OS | - | NA, | Nor, | RPE-1 |
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
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:49 Cells:% prod#:% Target#:38 State#:% Dir#:2
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