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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. |
| Breast Cancer |
| 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 |
| 5492- | EP, | Nano-Pulse Stimulation Therapy in Oncology |
| - | in-vivo, | PC, | Panc02 | - | in-vivo, | BC, | 4T1 |
| 4506- | GLA, | A basal level of γ-linolenic acid depletes Ca2+ stores and induces endoplasmic reticulum and oxidative stresses to cause death of breast cancer BT-474 cells |
| - | in-vitro, | BC, | BT474 |
| 1926- | JG, | Mechanism of juglone-induced apoptosis of MCF-7 cells by the mitochondrial pathway |
| - | in-vitro, | BC, | MCF-7 |
| 538- | MF, | The extremely low frequency electromagnetic stimulation selective for cancer cells elicits growth arrest through a metabolic shift |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | Melanoma, | MSTO-211H |
| 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 |
| 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 |
| 4354- | MF, | doxoR, | Modulated TRPC1 Expression Predicts Sensitivity of Breast Cancer to Doxorubicin and Magnetic Field Therapy: Segue Towards a Precision Medicine Approach |
| - | in-vivo, | BC, | MDA-MB-231 | - | in-vivo, | BC, | MCF-7 |
| 3491- | MFrot, | MF, | Magnetically controlled cyclic microscale deformation of in vitro cancer invasion models |
| - | in-vitro, | BC, | MDA-MB-231 |
| 2430- | PBG, | The cytotoxic effects of propolis on breast cancer cells involve PI3K/Akt and ERK1/2 pathways, mitochondrial membrane potential, and reactive oxygen species generation |
| - | in-vitro, | BC, | MDA-MB-231 |
| 4900- | Sal, | Anticancer Mechanisms of Salinomycin in Breast Cancer and Its Clinical Applications |
| - | Review, | BC, | 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 |
| 1751- | WBV, | Yoda1 Enhanced Low-Magnitude High-Frequency Vibration on Osteocytes in Regulation of MDA-MB-231 Breast Cancer Cell Migration |
| - | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | AML, | RAW264.7 |
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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