Database Query Results : Magnetic Fields, , angioG

MF, Magnetic Fields: Click to Expand ⟱
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


angioG, angiogenesis: Click to Expand ⟱
Source:
Type:
Process through which new blood vessels.
Angiogenesis, the process of new blood vessel formation from pre-existing vessels, plays a crucial role in cancer progression and metastasis. Tumors require a blood supply to grow beyond a certain size and to spread to other parts of the body.
Vascular Endothelial Growth Factor (VEGF): VEGF is one of the most important pro-angiogenic factors. It stimulates endothelial cell proliferation and migration, leading to the formation of new blood vessels. Many tumors overexpress VEGF, which correlates with poor prognosis.
Hypoxia-Inducible Factor (HIF): In response to low oxygen levels (hypoxia), tumors can activate HIF, which in turn promotes the expression of VEGF and other angiogenic factors. This mechanism allows tumors to adapt to their microenvironment and sustain growth.
Scientific Papers found: Click to Expand⟱
524- MF,    Inhibition of Angiogenesis Mediated by Extremely Low-Frequency Magnetic Fields (ELF-MFs)
- vitro+vivo, PC, MS-1 - vitro+vivo, PC, HUVECs
other↓, reduction of hemangioma size, of blood-filled spaces, and in hemorrhage.
TumCP↓,
TumCMig↓,
VEGFR2↓,
TumVol↓, 20mm compared to 32mm
HSP70/HSPA5↓, HSP70 and HSP90 expression after 72 h of exposure to MF in MS-1 cells seemed markedly reduced.
HSP90↓,
TumCCA↑, (2 mT) induced cell cycle arrest but not apoptosis. “transient” arrest of MF-treated cells in G2/M phase
angioG↓, in vitro

525- MF,    Pulsed electromagnetic fields regulate metabolic reprogramming and mitochondrial fission in endothelial cells for angiogenesis
- in-vitro, Nor, HUVECs
*angioG↑, PEMFs promoted a shift in the energy metabolism pattern of HUVECs from oxidative phosphorylation to aerobic glycolysis.
*GPx1↑, 4x
*GPx4↑, 2.2x
*SOD↑, SOD1/2 3.5x
*PFKM↑, 3x
*PFKL↑, 2.5x
*PKM2↑, 2.6x : activation of PKM2 enhanced angiogenesis in endothelial cells (ECs) by modulating glycolysis, mitochondrial fission, and fusion
*PFKP↑, 2.8x
*HK2↑, 4x
*GLUT1↑, 1.5x
*GLUT4↑, 1.6x
*ROS↓, reminder: normal HUVECs cells
*MMP↝, no damage, (normal cells)
*Glycolysis↑, (PFKL, PFKLM, PFKP, PKM2, and HK2) encoding the three key regulatory enzymes of glycolysis, hexokinase, phosphofructokinase, and pyruvate kinase, sharply increased when HUVECs were exposed to PEMFs
*OXPHOS↓, PEMFs promoted a shift in the energy metabolism pattern of HUVECs from oxidative phosphorylation to aerobic glycolysis

3465- MF,    Magnetic fields and angiogenesis
- Review, Var, NA
angioG↓, angiogenesis of tumor tissues can be inhibited by both static and dynamic magnetic fields at animal level.
*angioG↑, In contrast, long-term or high-intensity static magnetic field treatment of non-tumor tissue seems to be able to promote angiogenesis at animal level.
selectivity↑,
Ca+2↝, People speculate that magnetic field may regulate angiogenesis by affecting multiple signal transduction pathways including the calcium signaling pathway.
ROS↝, studies showing that other molecules could be involved in this process, including ROS (reactive oxygen species, ROS), ERK and membrane-bound receptors

3464- MF,    Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology
- Review, Var, NA
AntiTum↑, frequency below 300 Hz) exert anti-tumor function, independent of thermal effects
TumCG↓, Magnetic fields (MFs) could inhibit cell growth and proliferation; induce cell cycle arrest, apoptosis, autophagy, and differentiation; regulate the immune system; and suppress angiogenesis and metastasis via various signaling pathways
TumCCA↑,
Apoptosis↑,
TumAuto↑,
Diff↑,
angioG↓,
TumMeta↓,
EPR↑, MFs not only promote the absorption of chemotherapy drugs by producing small holes on the surface of cell membrane
ChemoSen↑,
ROS↑, MF treatment has been shown to promote the generation of ROS in many studies (31, 71, 72), with exposure within a 60 Hz sinusoidal MF for 48 h in induced human prostate cancer for DU145, PC3, and LNCaP apoptoses
DNAdam↑, Repetitive exposure to LF-MFs induced DNA damage and accumulation of DSBs and triggered apoptosis in Hela and MCF7 cell lines
P53↑, PMFs could trigger apoptosis cell death by upregulating the p53 level and through the mitochondrial-dependent pathway
Akt↓, LF-MFs (300 mT, 6 Hz, 24 h) also induced apoptosis by suppressing protein kinase B (Akt) signaling, activating p38 mitogen-activated protein kinase (MAPK) signaling, and caspase-9, which is the executor of the mitochondrial apoptosis pathway
MAPK↑,
Casp9↑,
VEGFR2↓, reducing the expression and activation levels of VEGFR2
P-gp↓, A combination with the SMF (8.8 m T, 12 h) decreased the expression of P-glycoprotein (P-gp) in K562 cancer cells, while adriamycin itself induced an increase

3466- MF,    The effect of magnetic fields on tumor occurrence and progression: Recent advances
- Review, Var, NA
angioG↓, magnetic fields suppress tumor angiogenesis, microcirculation, and enhance the immune response.
ROS↝, magnetic fields suppress tumors by interfering with DNA synthesis, reactive oxygen species level, second messenger molecule delivery, and orientation of epidermal growth factor receptors.
EGFR↝,
TumCG↓, increasing evidence that MFs can inhibit tumor progression, the underlying mechanism is still poorly understood

3467- MF,    Pulsed Magnetic Field Induces Angiogenesis and Improves Cardiac Function of Surgically Induced Infarcted Myocardium in Sprague-Dawley Rats
- in-vivo, Nor, NA
*angioG↑, 15 Hz 6 mT PMF promotes myocardial angiogenesis and improves cardiac function after MI in rats.
*cardioP↑,

509- MF,    Is extremely low frequency pulsed electromagnetic fields applicable to gliomas? A literature review of the underlying mechanisms and application of extremely low frequency pulsed electromagnetic fields
- Review, NA, NA
Ca+2↑,
TumAuto↑,
Apoptosis↑,
angioG↓,
ROS↑,

499- MF,    The Effect of Pulsed Electromagnetic Fields on Angiogenesis
- Review, NA, NA
angioG↑, normal tissue
VEGF↑, normal tissue
VGCC↑, normal tissue

4092- MF,    Mechanisms and therapeutic effectiveness of pulsed electromagnetic field therapy in oncology
- Review, Var, NA
Apoptosis↑, 20 Hz; 3 mT, 60mins/day PEMFs increased apoptosis in MCF7 cells but had no effect on MCF10 cells
selectivity↑,
ROS↑, 50 Hz, 0.1–1.0 mT) for 30 min, and long‐term PEMF: undifferentiated PC12 cells increased ROS levels and decreased catalase activity
Catalase↓,
TumVol↓, 1 Hz, 100 mT, Mice exposed for 60 and 180 min daily showed a 30% and 70% tumor reduction
angioG↓, PEMFs inhibit angiogenesis in tumor tissues, suppressing tumor vascularization and reducing tumor growth, as shown by in vivo studies

3477- MF,    Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis
- Review, NA, NA
*Ca+2↑, When cells are subjected to external mechanical stimulation, voltage-gated ion channels in the cell membrane open and intracellular calcium ion concentration rises
*VEGF↑, BMSCs EMF combined with VEGF promote osteogenesis and angiogenesis
*angioG↑,
Ca+2↑, 1 Hz/100 mT MC4-L2 breast cancer cells EMF lead to calcium ion overload and ROS increased, resulting in necroptosis
ROS↑,
Necroptosis↑,
TumCCA↑, 50 Hz/4.5 mT 786-O cells ELF-EMF induce G0/G1 arrest and apoptosis in cells lines
Apoptosis↑,
*ATP↑, causing the ATP or ADP increases, and the purinergic signal can upregulate the expression of P2Y1 receptors
*FAK↑, Our research team [53] found that ELE-EMF can induce calcium oscillations in bone marrow stem cells, up-regulated calcium ion activates FAK pathway, cytoskeleton enhancement, and migration ability of stem cells in vitro is enhanced.
*Wnt↑, ability of EMF to activate the Wnt10b/β-catenin signaling pathway to promote osteogenic differentiation of cells depends on the functional integrity of primary cilia in osteoblasts.
*β-catenin/ZEB1↑,
*ROS↑, we hypothesize that the electromagnetic field-mediated calcium ion oscillations, which causes a small amount of ROS production in mitochondria, regulates the chondrogenic differentiation of cells, but further studies are needed
p38↑, RF-EMF was able to suppress tumor stem cells by activating the CAMKII/p38 MAPK signaling pathway after inducing calcium ion oscillation and by inhibiting the β-catenin/HMGA2 signaling pathway
MAPK↑,
β-catenin/ZEB1↓,
CSCs↓, Interestingly, the effect of electromagnetic fields is not limited to tumor stem cells, but also inhibits the proliferation and development of tumor cells
TumCP↓,
ROS↑, breast cancer cell lines exposed to ELE-EMF for 24 h showed a significant increase in intracellular ROS expression and an increased sensitivity to further radiotherapy
RadioS↑,
Ca+2↑, after exposure to higher intensity EMF radiation, showed a significant increase in intracellular calcium ion and reactive oxygen species, which eventually led to necroptosis
eff↓, while this programmed necrosis of tumor cells was able to be antagonized by the calcium blocker verapamil or the free radical scavenger n -acetylcysteine
NO↑, EMF can regulate multiple ions in cells, and calcium ion play a key role [92, 130], calcium ion acts as a second messenger that can activate downstream molecules such as NO, ROS

3478- MF,    One Month of Brief Weekly Magnetic Field Therapy Enhances the Anticancer Potential of Female Human Sera: Randomized Double-Blind Pilot Study
- Trial, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, C2C12
TumCP↓, Female sera from the magnetic therapy group (n = 12) reduced breast cancer cell proliferation (16.1%), migration (11.8%) and invasion (28.2%) and reduced the levels of key EMT markers relative to the control sera
TumCMig↓,
TumCI↓,
*toxicity∅, The provision of week 5 or week 8 PEMF sera to MCF10A cells did not alter their viability, being comparable to that observed with the control sera (
TGF-β↓, The week 8 PEMF sera resulted in the significant downregulation of (A) TGFβR2, (B) TWIST, (C) SNAI1, (D) SNAI2 (Slug), (E) β-catenin and (F) Vimentin protein expressions, when compared to week 8 control sera
Twist↓,
Slug↓,
β-catenin/ZEB1↓,
Vim↓,
p‑SMAD2↓, Week 5 PEMF sera primarily reduced the phosphorylation of SMAD 2/3 as well as the expression of TWIST protein expression.
p‑SMAD3↓,
angioG↓, Week 8 PEMF-plasma showed significant reductions in angiogenic biomarkers, including Angiopoietin-2, BMP-9, Endoglin, PLGF, VEGF-A, and VEGF-D
VEGF↓,
selectivity↑, PEMF sera did not adversely alter the growth of non-malignant cells such as MCF10A (breast epithelial) and C2C12 (myogenic).
LIF↑, Similarly, LIF (leukemia inhibitory factor) was upregulated one week after the final PEMF treatment.

3482- MF,    Pulsed Electromagnetic Fields Increase Angiogenesis and Improve Cardiac Function After Myocardial Ischemia in Mice
- in-vitro, NA, NA
*cardioP↑, PEMF treatment with 30 Hz 3.0 mT significantly improved heart function.
*VEGF↑, PEMF treatment with 15 Hz 1.5 mT and 30 Hz 3.0 mT both increased capillary density, decreased infarction area size, increased the protein expression of vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 2 (VEGFR2
*VEGFR2↑,
*Hif1a↑, and increased the mRNA level of VEGF and hypoxia inducible factor 1-alpha (HIF-1α) in the infarct border zone.
*FGF↑, Additionally, treatment with 30 Hz 3.0 mT also increased protein and mRNA level of fibroblast growth factor 2 (FGF2), and protein level of β1 integrin, and shows a stronger therapeutic effect.
*ITGB1↑,
*angioG↑, PEMFs Improve Angiogenesis In Vivo

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
*Inflam↓, (PEMF), a biophysical form of stimulation, has an anti-inflammatory effect by causing differentiation of MSCs.
*Diff↑,
*toxicity∅, PEMF have been reported to last up to 3 months or longer in human patients with chronic inflammatory/autoimmune disorders (38) with no evidence of adverse effects (39).
*other↑, MSCs to promote immunomodulation and improve cartilage and bone regeneration in vitro (10) and in vivo (73).
*SOX9↑, enhanced chondrogenic gene expression in SOX-9, COL II, and aggrecan in MSCs
*COL2A1↑,
*NO↓, Prevented increases in NO
*PGE2↓, Exposure to PEMF induces early upregulation of adenosine receptors A2A and A3 that reduce PGE2 and pro-inflammatory cytokines such as TNF-α, which combine to inhibit the activation of transcription factor NF-kB
*NF-kB↓,
*TNF-α↓, 1 h exposure to PEMF has been shown to down-regulate both NF-kB and TNF-α in murine macrophages
*IL1β↓, By inhibiting NF-kB activation (94), exposure to PEMF led to decreased production of TNF-α, IL-1β, IL-6, and PGE2 in human chondrocytes, osteoblasts, and synovial fibroblasts
*IL6↓,
*IL10↑, Inhibited release of PGE2, and IL-1β and IL-6 production, while stimulating release of IL-10 in synovial fibroblasts
*angioG↑, progenitor cells (EPCs) to an RA injury site is important for repair of vasculature and angiogenesis. PEMF has also been reported to increase the number and function of circulating EPCs in treating myocardial ischemia/reperfusion (I/R) injury in rat
*MSCs↑, Since PEMF have been shown to stimulate the production of MSCs
*VEGF↑, promoting the expression of growth factors such as VEGF and TGF-β
*TGF-β↑,
*angioG↝, modulate the aberrant angiogenesis present in RA: reported to significantly reduce activation levels of VEGF (15), to inhibit the proliferative ability of HUVECs, and to reduce the extent of vascularization in diseased tissue
*VEGF↓, diseased tissue
Ca+2↝, By restoring normal Ca2+ ion flux and Na+/K+ balance, the cell can begin the process of down-regulating inflammatory cytokines, HSPs, and proangiogenic molecules such as VEGF, making it possible for the body to commence rebuilding healthy cartilage.

3497- MFrot,  MF,    The Effect of a Rotating Magnetic Field on the Regenerative Potential of Platelets
- Human, Nor, NA
*PDGFR-BB↑, The highest concentration of PDGF-BB was observed in the samples placed in RMF for 1 h at 25 Hz
*TGF-β↑, For TGF-β1, the highest concentrations were obtained in the samples exposed to RMF for 3 h at 25 Hz and 1 h at 50 Hz.
*IGF-1↑, highest concentrations of IGF-1 and FGF-1 were shown in plasma placed in RMF for 3 h at 25 Hz.
*FGF↑,
*angioG↑, Magnetic fields have been shown to have a beneficial effect on vasodilation, angiogenesis, accelerating repair, regeneration, and healing of soft tissues, nervous tissues and bones, analgesic aspects, anti-swelling, reducing inflammation and pain, an
*Inflam↓,
*ROS↓, RMF exposure can increase resistance to heat stress, reduce levels of ROS, affect intracellular calcium ion concentrations, and contribute to cell aging deceleration


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 14

Results for Effect on Cancer/Diseased Cells:
Akt↓,1,   angioG↓,7,   angioG↑,1,   AntiTum↑,1,   Apoptosis↑,4,   Ca+2↑,3,   Ca+2↝,2,   Casp9↑,1,   Catalase↓,1,   ChemoSen↑,1,   CSCs↓,1,   Diff↑,1,   DNAdam↑,1,   eff↓,1,   EGFR↝,1,   EPR↑,1,   HSP70/HSPA5↓,1,   HSP90↓,1,   LIF↑,1,   MAPK↑,2,   Necroptosis↑,1,   NO↑,1,   other↓,1,   P-gp↓,1,   p38↑,1,   P53↑,1,   RadioS↑,1,   ROS↑,5,   ROS↝,2,   selectivity↑,3,   Slug↓,1,   p‑SMAD2↓,1,   p‑SMAD3↓,1,   TGF-β↓,1,   TumAuto↑,2,   TumCCA↑,3,   TumCG↓,2,   TumCI↓,1,   TumCMig↓,2,   TumCP↓,3,   TumMeta↓,1,   TumVol↓,2,   Twist↓,1,   VEGF↓,1,   VEGF↑,1,   VEGFR2↓,2,   VGCC↑,1,   Vim↓,1,   β-catenin/ZEB1↓,2,  
Total Targets: 49

Results for Effect on Normal Cells:
angioG↑,7,   angioG↝,1,   ATP↑,1,   Ca+2↑,1,   cardioP↑,2,   COL2A1↑,1,   Diff↑,1,   FAK↑,1,   FGF↑,2,   GLUT1↑,1,   GLUT4↑,1,   Glycolysis↑,1,   GPx1↑,1,   GPx4↑,1,   Hif1a↑,1,   HK2↑,1,   IGF-1↑,1,   IL10↑,1,   IL1β↓,1,   IL6↓,1,   Inflam↓,2,   ITGB1↑,1,   MMP↝,1,   MSCs↑,1,   NF-kB↓,1,   NO↓,1,   other↑,1,   OXPHOS↓,1,   PDGFR-BB↑,1,   PFKL↑,1,   PFKM↑,1,   PFKP↑,1,   PGE2↓,1,   PKM2↑,1,   ROS↓,2,   ROS↑,1,   SOD↑,1,   SOX9↑,1,   TGF-β↑,2,   TNF-α↓,1,   toxicity∅,2,   VEGF↓,1,   VEGF↑,3,   VEGFR2↑,1,   Wnt↑,1,   β-catenin/ZEB1↑,1,  
Total Targets: 46

Scientific Paper Hit Count for: angioG, angiogenesis
14 Magnetic Fields
1 Magnetic Field Rotating
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:172  Target#:447  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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