| 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↑, 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 Non-Static Magnetic Fields (AC / Pulsed / Oscillating MF)
Time-Scale Flag: TSF = P / R / G P: 0–30 min (physical / electron / radical effects) R: 30 min–3 hr (redox signaling & stress response) G: >3 hr (gene-regulatory adaptation)MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure. |
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| Also known as CP32. Cysteinyl aspartate specific proteinase-3 (Caspase-3) is a common key protein in the apoptosis and pyroptosis pathways, and when activated, the expression level of tumor suppressor gene Gasdermin E (GSDME) determines the mechanism of tumor cell death. As a key protein of apoptosis, caspase-3 can also cleave GSDME and induce pyroptosis. Loss of caspase activity is an important cause of tumor progression. Many anticancer strategies rely on the promotion of apoptosis in cancer cells as a means to shrink tumors. Crucial for apoptotic function are executioner caspases, most notably caspase-3, that proteolyze a variety of proteins, inducing cell death. Paradoxically, overexpression of procaspase-3 (PC-3), the low-activity zymogen precursor to caspase-3, has been reported in a variety of cancer types. Until recently, this counterintuitive overexpression of a pro-apoptotic protein in cancer has been puzzling. Recent studies suggest subapoptotic caspase-3 activity may promote oncogenic transformation, a possible explanation for the enigmatic overexpression of PC-3. Herein, the overexpression of PC-3 in cancer and its mechanistic basis is reviewed; collectively, the data suggest the potential for exploitation of PC-3 overexpression with PC-3 activators as a targeted anticancer strategy. Caspase 3 is the main effector caspase and has a key role in apoptosis. In many types of cancer, including breast, lung, and colon cancer, caspase-3 expression is reduced or absent. On the other hand, some studies have shown that high levels of caspase-3 expression can be associated with a better prognosis in certain types of cancer, such as breast cancer. This suggests that caspase-3 may play a role in the elimination of cancer cells, and that therapies aimed at activating caspase-3 may be effective in treating certain types of cancer. Procaspase-3 is a apoptotic marker protein. Prognostic significance: • High Cas3 expression: Associated with good prognosis and increased sensitivity to chemotherapy in breast, gastric, lung, and pancreatic cancers. • Low Cas3 expression: Linked to poor prognosis and increased risk of recurrence in colorectal, hepatocellular carcinoma, ovarian, and prostate cancers. |
| 400- | AgNPs, | 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 |
| 401- | GoldNP, | MF, | In vitro evaluation of electroporated gold nanoparticles and extremely-low frequency electromagnetic field anticancer activity against Hep-2 laryngeal cancer cells |
| - | in-vitro, | Laryn, | HEp2 |
| 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 |
| 497- | MF, | In Vitro and in Vivo Study of the Effect of Osteogenic Pulsed Electromagnetic Fields on Breast and Lung Cancer Cells |
| - | vitro+vivo, | NA, | MCF-7 | - | vitro+vivo, | NA, | A549 |
| 496- | MF, | Low-Frequency Magnetic Fields (LF-MFs) Inhibit Proliferation by Triggering Apoptosis and Altering Cell Cycle Distribution in Breast Cancer Cells |
| - | in-vitro, | BC, | MCF-7 | - | in-vitro, | BC, | ZR-75-1 | - | in-vitro, | BC, | T47D | - | in-vitro, | BC, | MDA-MB-231 |
| 194- | MF, | Electromagnetic Field as a Treatment for Cerebral Ischemic Stroke |
| - | Review, | Stroke, | NA |
| 506- | MF, | doxoR, | Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in Doxorubicin-treated Mouse Osteosarcoma Cells |
| - | in-vitro, | OS, | LM8 |
| 4147- | MF, | PEMFs Restore Mitochondrial and CREB/BDNF Signaling in Oxidatively Stressed PC12 Cells Targeting Neurodegeneration |
| - | in-vitro, | AD, | PC12 |
| 2259- | MFrot, | MF, | Method and apparatus for oncomagnetic treatment |
| - | in-vitro, | GBM, | NA |
| 198- | MFrot, | MF, | Biological effects of rotating magnetic field: A review from 1969 to 2021 |
| - | Review, | Var, | NA |
| 186- | MFrot, | MF, | Selective induction of rapid cytotoxic effect in glioblastoma cells by oscillating magnetic fields |
| - | in-vitro, | GBM, | GBM | - | in-vitro, | Lung, | NA |
| 188- | MFrot, | MF, | Spinning magnetic field patterns that cause oncolysis by oxidative stress in glioma cells |
| - | in-vitro, | GBM, | GBM115 | - | in-vitro, | GBM, | DIPG |
| 184- | MFrot, | MF, | Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells |
| - | in-vitro, | GBM, | GBM |
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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