| Features: Therapy |
| Magnetic Fields can be Static, or pulsed. The most common therapy is a pulsed magnetic field in the uT or mT range. The main pathways affected are: Calcium Signaling: -influence the activity of voltage-gated calcium channels. Oxidative Stress and Reactive Oxygen Species (ROS) Pathways Heat Shock Proteins (HSPs) and Cellular Stress Responses Cell Proliferation and Growth Signaling: MAPK/ERK pathway. Gene Expression and Epigenetic Modifications: NF-κB Angiogenesis Pathways: VEGF (improving VEGF for normal cells) PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models Pathways: - most reports have ROS production increasing in cancer cells , while decreasing in normal cells. - ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑">Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx, - Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : NLRP3↓, IL-1β↓, TNF-α↓, IL-6↓, IL-8↓ - inhibit Growth/Metastases : TumMeta↓, TumCG↓, VEGF↓(mostly regulated up in normal cells), - cause Cell cycle arrest : TumCCA↑, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, - inhibits glycolysis /Warburg Effect and ATP depletion : HIF-1α↓, PKM2↓, GLUT1↓, LDH↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓ - inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, FGF↓, PDGF↓, EGFR↓, Integrins↓, - Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, ERK↓, JNK, - SREBP (related to cholesterol). - Synergies: chemo-sensitization, chemoProtective, cytoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Hepatoprotective, CardioProtective, - Selectivity: Cancer Cells vs Normal Cells |
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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. |
| 2018- | CAP, | MF, | Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma |
| - | Review, | HCC, | NA |
| 2250- | MF, | MNPs, | Confronting stem cells with surface-modified magnetic nanoparticles and low-frequency pulsed electromagnetic field |
| - | Review, | NA, | NA |
| 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 |
| 2239- | MF, | Time-varying magnetic fields increase cytosolic free Ca2+ in HL-60 cells |
| - | in-vitro, | AML, | HL-60 |
| 2238- | MF, | Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects |
| - | Review, | Var, | 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 |
| 2236- | MF, | Changes in Ca2+ release in human red blood cells under pulsed magnetic field |
| - | in-vitro, | Nor, | NA |
| 2235- | MF, | Increase of intracellular Ca2+ concentration in Listeria monocytogenes under pulsed magnetic field |
| - | in-vitro, | Inf, | NA |
| 1762- | MF, | Fe, | Triggering the apoptosis of targeted human renal cancer cells by the vibration of anisotropic magnetic particles attached to the cell membrane |
| - | in-vitro, | RCC, | NA |
| 3487- | MF, | Rad, | High-specificity protection against radiation-induced bone loss by a pulsed electromagnetic field |
| - | Review, | Var, | NA |
| 3480- | MF, | Cellular and Molecular Effects of Magnetic Fields |
| - | Review, | NA, | NA |
| 3501- | MF, | Unveiling the Power of Magnetic-Driven Regenerative Medicine: Bone Regeneration and Functional Reconstruction |
| - | Review, | NA, | NA |
| 3536- | MF, | Targeting Mesenchymal Stromal Cells/Pericytes (MSCs) With Pulsed Electromagnetic Field (PEMF) Has the Potential to Treat Rheumatoid Arthritis |
| - | Review, | Arthritis, | NA | - | Review, | Stroke, | NA |
| 2261- | MF, | Tumor-specific inhibition with magnetic field |
| - | in-vitro, | Nor, | GP-293 | - | in-vitro, | Liver, | HepG2 | - | in-vitro, | Lung, | A549 |
| 3477- | MF, | Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis |
| - | Review, | NA, | NA |
| 3469- | MF, | Pulsed Electromagnetic Fields (PEMF)—Physiological Response and Its Potential in Trauma Treatment |
| - | Review, | NA, | NA |
| 3458- | MF, | Magnetic Control of Protein Expression via Magneto-mechanical Actuation of ND-PEGylated Iron Oxide Nanocubes for Cell Therapy |
| - | in-vitro, | GBM, | NA |
| 3457- | MF, | Cellular stress response to extremely low‐frequency electromagnetic fields (ELF‐EMF): An explanation for controversial effects of ELF‐EMF on apoptosis |
| - | Review, | Var, | NA |
| 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 |
| 503- | MF, | Effects of acute and chronic low frequency electromagnetic field exposure on PC12 cells during neuronal differentiation |
| - | in-vitro, | NA, | PC12 |
| 506- | MF, | doxoR, | Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in Doxorubicin-treated Mouse Osteosarcoma Cells |
| - | in-vitro, | OS, | LM8 |
| - | Review, | NA, | NA |
| 194- | MF, | Electromagnetic Field as a Treatment for Cerebral Ischemic Stroke |
| - | Review, | Stroke, | NA |
| 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 |
| 537- | MF, | immuno, | Integrating electromagnetic cancer stress with immunotherapy: a therapeutic paradigm |
| - | Review, | Var, | NA |
| 535- | MF, | Electromagnetic Fields Trigger Cell Death in Glioblastoma Cells through Increasing miR-126-5p and Intracellular Ca2+ Levels |
| - | in-vitro, | Pca, | PC3 | - | in-vitro, | GBM, | A172 | - | in-vitro, | Pca, | HeLa |
| 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 |
| 529- | MF, | Low-frequency magnetic field therapy for glioblastoma: Current advances, mechanisms, challenges and future perspectives |
| - | Review, | GBM, | NA |
| 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 |
| 528- | MF, | Caff, | Pulsed electromagnetic fields affect the intracellular calcium concentrations in human astrocytoma cells |
| - | in-vitro, | GBM, | U373MG |
| 400- | SNP, | MF, | Polyvinyl Alcohol Capped Silver Nanostructures for Fortified Apoptotic Potential Against Human Laryngeal Carcinoma Cells Hep-2 Using Extremely-Low Frequency Electromagnetic Field |
| - | in-vitro, | Laryn, | HEp2 |
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