Magnetic Fields Cancer Research Results

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">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)
Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Reactive oxygen species (ROS) ↑ ROS (P→R); often sustained (G) ↑ ROS (P); ↔/↓ net ROS (R→G) P, R, G Upstream redox perturbation MF perturbs electron/radical dynamics: normal cells often adapt (ROS setpoint ↓), cancer cells less so
2 NRF2 antioxidant response ↔ / insufficient NRF2 induction (R→G) ↑ NRF2 activation (R→G) R, G Adaptive redox defense Explains mixed ROS direction in normal cells (initial ↑ then adaptive ↓)
3 Glutathione (GSH) homeostasis ↓ GSH (R→G) ↔ or transient ↓ (R) with recovery (G) R, G Redox buffering capacity GSH depletion reflects sustained oxidative load; recovery indicates successful adaptation
4 Superoxide dismutase (SOD) / antioxidant enzymes ↔ or inadequate enzyme upshift (G) ↑ SOD/GPx/CAT capacity (G) G Longer-term antioxidant remodeling Often the “endpoint” readout that correlates with ROS-normalization in normal tissue
5 Mitochondrial ETC / respiration ↓ ETC efficiency; ↑ electron leak (P→R) ↔ mild, reversible ETC perturbation (P→R) P, R Bioenergetic destabilization ETC perturbation is a mechanistic bridge between MF exposure and ROS/ΔΨm changes
6 Mitochondrial membrane potential (ΔΨm / MMP) ↓ ΔΨm (R); may progress (G) ↔ preserved or reversible dip (R) R, G Mitochondrial dysfunction thresholding ΔΨm loss typically follows ROS/ETC disruption rather than preceding it
7 Ca²⁺ signaling (VGCC / ER–mitochondria Ca²⁺ flux) ↑ dysregulated Ca²⁺ influx/transfer (P→R); overload may persist (G) ↑ transient Ca²⁺ signaling (P); homeostasis restored (R→G) P, R, G Stress signal amplification Ca²⁺ dysregulation links ROS/ETC perturbation to ER stress and mitochondrial dysfunction (amplifies ΔΨm loss and UPR commitment)
8 Mitochondrial permeability transition pore (MPTP) ↑ MPTP opening propensity (R); sustained opening possible (G) ↔ transient or closed (R→G) P, R, G Commitment point for mitochondrial failure MPTP opening integrates ROS, Ca²⁺ overload, and ΔΨm loss; acts as a threshold event converting reversible stress into irreversible mitochondrial dysfunction
9 ER stress / UPR ↑ ER stress (R); CHOP-commitment possible (G) ↑ adaptive UPR (R); resolves (G) R, G Proteostasis stress Often downstream of ROS + Ca²⁺ handling perturbations
10 DNA damage (oxidative) ↑ damage markers (R→G) ↔ or repaired (G) R, G Checkpoint pressure Generally secondary to ROS; interpret as stress consequence not “direct genotoxicity”
11 LDH / glycolytic flux ↓ glycolytic performance (R→G) ↔ flexible substrate switching (R→G) R, G Metabolic vulnerability Redox imbalance can destabilize high-rate glycolysis in cancer-biased contexts
12 Thioredoxin system (Trx / TrxR) ↓ functional reserve / overload (R→G) ↔ preserved capacity (G) R, G Parallel antioxidant system stress Useful when GSH-only does not explain redox phenotype 
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.
Scientific Papers found: Click to Expand⟱
356- AgNPs,  MF,    Anticancer and antibacterial potentials induced post short-term exposure to electromagnetic field and silver nanoparticles and related pathological and genetic alterations: in vitro study
- in-vitro, BC, MCF-7 - in-vitro, Bladder, HTB-22
Apoptosis↑,
P53↑, Up-regulation in the expression level of p53, iNOS and NF-kB genes as well as down-regulation of Bcl-2 and miRNA-125b genes were detected post treatment.
iNOS↑,
NF-kB↑,
Bcl-2↓,
ROS↑, the present study evaluated the levels of ROS as well as the antioxidant enzymes (SOD and CAT)
SOD↑,
TumCCA↑, S phase arrest and accumulation of cells in G2/M phase was observed following exposure to AgNPs and EMF, respectively.
eff↑, Apoptosis induction was obvious following exposure to either ELF-EMF or AgNPs, however their apoptotic potential was intensified when applied in combination
Catalase↑, Catalase (CAT)
other↑, swollen cells, swollen nuclei with mixed euchromatin and heterochromatin, ruptured cell membranes

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
TumCP↓, especially in the G0/G1 and S phases.
Casp3↑,
P53↑,
Beclin-1↑,
TumAuto↑,
GSR↑, oxidative stress biomarker
ROS↑, oxidative stress biomarker
MDA↑, oxidative stress biomarker
ROS↑,
SIRT1↑,
Ca+2↑, induce apoptosis in osteoclasts by increasing intracellular and nucleus Ca2+ concentration
Endon↑, increases endonuclease activity
DNAdam↑,
Apoptosis↑,
NF-kB↓,

402- AgNPs,  MF,    Anticancer and antibacterial potentials induced post short-term exposure to electromagnetic field and silver nanoparticles and related pathological and genetic alterations: in vitro study
- in-vitro, BC, MCF-7
P53↑,
iNOS↑,
NF-kB↑,
Bcl-2↓,
miR-125b↓,
ROS↑, 2.9x for 2hr
SOD↑, 2.4x for 2hr

2612- Ba,  MF,    The effect of a static magnetic field and baicalin or baicalein interactions on amelanotic melanoma cell cultures (C32)
- in-vitro, Melanoma, NA
SOD1↑, Baicalein ONLY: increase in the expression of the SOD1 , SOD2 and GPX1 genes compared to the nontreated cell cultures
SOD2↑,
GPx1↑,
Dose?, A chamber with a field induction of 0.7 T was used for the tests
eff↝, There was no significant difference in the expression of the SOD1, SOD2 or GPX1 genes in the melanoma cell cultures that had only been exposed to a static magnetic field (0.7 T)
SOD1↓, Baicalein + 0.7T MF: decreases SOD1 , SOD2 and GPX1
SOD2↓,
GPx1↓,

2018- CAP,  MF,    Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma
- Review, HCC, NA
TRPV1↑, Capsaicin is an agonist for transient receptor potential cation channel subfamily V member 1 (TRPV1)
eff↑, It is noteworthy that capsaicin binding to the TRPV1 receptor may be increased using a static magnetic field (SMF), thus enhancing the anti-cancer effect of capsaicin on HepG2 (human hepatoblastoma cell line) cells through caspase-3 apoptosis
Akt↓, capsaicin can regulate autophagy by inhibiting the Akt/mTOR
mTOR↓,
p‑STAT3↑, Capsaicin can upregulate the activity of the signal transducer and activator of transcription 3 (p-STAT3)
MMP2↑, increase of the expression of MMP-2
ER Stress↑, capsaicin may induce apoptosis through endoplasmic reticulum (ER) stress
Ca+2↑, and the subsequent ER release of Ca2+
ROS↑, Capsaicin-induced ROS generation
selectivity↑, On the other hand, an excess of capsaicin is cytotoxic on HepG2 cells, and normal hepatocytes to a smaller extent, by collapse of the mitochondrial membrane potential with ROS formation
MMP↓,
eff↑, combination of capsaicin and sorafenib demonstrated significant anticarcinogenic properties on LM3 HCC cells, restricting tumor cell growth

659- EGCG,  MNPs,  MF,    Augmented cellular uptake of nanoparticles using tea catechins: effect of surface modification on nanoparticle-cell interaction
- in-vivo, Nor, NA
*BioEnh↑, EGCG at a concentration as low as 1-3 μM, which increased MNP uptake 2- to 7-fold. In addition, application of magnetic force further potentiated MNP uptake, suggesting a synergetic effect of EGCG and magnetic force

658- EGCG,  MNPs,  MF,    Laminin Receptor-Mediated Nanoparticle Uptake by Tumor Cells: Interplay of Epigallocatechin Gallate and Magnetic Force at Nano-Bio Interface
- in-vitro, GBM, LN229
*BioEnh↑, (EGCG), a major tea catechin, enhances cellular uptake of magnetic nanoparticles (MNPs

657- EGCG,  MNPs,  MF,    Interaction of poly-l-lysine coating and heparan sulfate proteoglycan on magnetic nanoparticle uptake by tumor cells
- in-vitro, GBM, U87MG
*BioEnh↑, enhances MNP internalization by 3.1-fold

654- EGCG,  MNPs,  MF,    Characterization of mesenchymal stem cells with augmented internalization of magnetic nanoparticles: The implication of therapeutic potential
- in-vitro, Var, NA
*BioEnh↑, (EGCG) has been known to greatly enhance MNP uptake by tumor cells

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
Casp3↑,
P53↑,
BAX↑,
Bcl-2↓,

539- MF,    Pulsed Magnetic Field Improves the Transport of Iron Oxide Nanoparticles through Cell Barriers
- in-vitro, NA, NA
eff↑, enchanced Magnetic NP uptake

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
TumCG↓, did not affect the non-malignant counterpart.
Ca+2↑,
COX2↓,
ATP↑, (ATP5B) and mitochondrial transcription (MT-ATP6)
MMP↑, significant enhancement of mitochondrial membrane potential (ΔΨm)
ROS↑, demonstrated for the first time the association of ROS production with the stimulation of the mitochondrial metabolism triggered by the electromagnetic field
OXPHOS↑,
mitResp↑, Mitochondrial respiration is increased by ELF-EMF exposure

582- MF,  immuno,  VitC,    Magnetic field boosted ferroptosis-like cell death and responsive MRI using hybrid vesicles for cancer immunotherapy
- in-vitro, Pca, TRAMP-C1 - in-vivo, NA, NA
Fenton↑, boost, Ascorbic acid (AA, C6H8O6) can act as an electron-donor
Ferroptosis↑, HCSVs and MF efficiently inhibited TRAMP-C1 growth through ferroptosis-mediated cell death.
ROS↑, The generated ferrous ions, inducing stronger Fenton-like oxidation than ferric ions, triggered the higher accumulation of ROS, and finally inhibited tumor cell growth
TumCG↓, Collectively, it was proved that the exogenous magnetic field-boosted Fenton reaction efficiently inhibit tumor growth.
Iron↑, after 10-min MF treatment, the increase of ferrous ions was found in 0.1 h
GPx4↓, combination treatment of MF and HCSVs downregulated GPX4

585- MF,  VitC,    Impact of pulsed magnetic field treatment on enzymatic inactivation and quality of cloudy apple juice
other↓, significant decreases of ascorbic acid were observed at the intensity of 7 T with 5–30 pulses.

587- MF,  VitC,    Effect of stationary magnetic field strengths of 150 and 200 mT on reactive oxygen species production in soybean
ROS↑,
SOD↓,
other↓, ascorbic acid content decreased

590- MF,  VitC,    Sub-millitesla magnetic field effects on the recombination reaction of flavin and ascorbic acid radicals
- in-vitro, NA, NA
RPM↑,

592- MF,  VitC,    Alternative radical pairs for cryptochrome-based magnetoreception
RPM↑,

594- MF,  VitC,    Static Magnetic Field Effect on the Fremy's Salt-Ascorbic Acid Chemical Reaction Studied by Continuous-Wave Electron Paramagnetic Resonance
- Analysis, NA, NA
RPM↑,

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
Dose∅, low frequencies (∼20 Hz) and in weak magnetic fields (∼30 mT)
Apoptosis↑, triggering of the apoptosis of these cancer cells was demonstrated with NiFe vortex particles and statistically characterized by flow-cytometry studies
Casp↑,
tumCV↓, In conclusion, a decrease of ~70% in viable cells was observed only six hours after the magneto-mechanical stimulus treatment
Casp3↑, microdisk vibrations initiated the intracellular cascade that leads to effector caspase 3/7 activation.
Casp7↑,
Ca+2↑, mechanotransduction leads to an increase of the intracellular Ca 2+ ions which serve as downstream signaling elements that propagate and amplify the apoptosis
Cyt‑c↑, The targets of such a signaling pathway include the cytochrome C release

2235- MF,    Increase of intracellular Ca2+ concentration in Listeria monocytogenes under pulsed magnetic field
- in-vitro, Inf, NA
Ca+2↑, Intracellular Ca2+ concentration in L. monocytogenes increased after PMF treatment.
TumCD↑, The death of L. monocytogenes treated by PMF might be related to the increase of intracellular Ca2+ concentration.

2236- MF,    Changes in Ca2+ release in human red blood cells under pulsed magnetic field
- in-vitro, Nor, NA
*Ca+2↓, Pulsed magnetic field (PMF) decreases Ca2+ level of inner red blood cell (RBC).
*eff↓, PMF gives RBCs positive effect consistently in Ca2+ level and plays a role in preventing RBC hemolysis from oxidative stress and improving RBCD.
*ROS↓, PMF plays a role in preventing oxidative stress or in restoring oxidative stress on RBCs.

529- MF,    Low-frequency magnetic field therapy for glioblastoma: Current advances, mechanisms, challenges and future perspectives
- Review, GBM, NA
Ca+2↑, U-373MG 50 Hz, 3 mT 24 h Increased the intracellular Ca2+
ROS↑, BT115, U87, BT175 50–350 Hz, 1–58 mT 2–4 h Increased the ROS level and cell death
ChemoSen↑, A growing amount of evidence has validated that LF-MFs combined with chemotherapeutic drugs have a synergistic effect in the treatment of GBM
QoL↑, For example, researchers have discovered that LF-MFs can improve the quality of life of patients with recurrent GBM
OS↑, clinical trials have also validated the excellent therapeutic efficacy of LF-MFs in prolonging OS and improving quality of life in GBM patients

519- MF,    Effects of 50-Hz magnetic field exposure on superoxide radical anion formation and HSP70 induction in human K562 cells
- in-vitro, AML, K562
HSP70/HSPA5↑, 2x

520- MF,    Exposure to a 50-Hz magnetic field induced mitochondrial permeability transition through the ROS/GSK-3β signaling pathway
- in-vitro, Nor, NA
*MPT↑, MPT induced by MF exposure was mediated through the ROS/GSK-3β signaling pathway.
*Cyt‑c↑, induced Cyt-c release
*ROS↑, cells exposed to the MF showed increased intracellular reactive oxidative species (ROS) levels and glycogen synthase kinase-3β (GSK-3β) dephosphorylation at 9 serine residue (Ser(9))
*p‑GSK‐3β↑,
*eff↓, attenuated by ROS scavenger (N-acetyl-L-cysteine, NAC) or GSK-3β inhibitor
*MMP∅, no significant effect on mitochondrial membrane potential (ΔΨm)
*BAX↓, Bax declined around 15% which was statistically significant while the total level of Bcl-2 reminded unchanged in cells
*Bcl-2∅,

521- MF,    Magnetic field effects in biology from the perspective of the radical pair mechanism
- Analysis, NA, NA
*RPM↑, Due to the spin interactions with its environment (in particular with external magnetic fields and with nearby nuclear spins), the state of the radical pair will oscillate between S and T states
*ROS↝, The effects of oscillating magnetic fields on biological functions are abundant [207–215], and are often correlated with modulation of ROS levels

523- MF,  MTX,    Extremely low-frequency magnetic fields significantly enhance the cytotoxicity of methotrexate and can reduce migration of cancer cell lines via transiently induced plasma membrane damage
- in-vitro, AML, THP1 - in-vitro, NA, PC12 - in-vivo, Cerv, HeLa
H2O2↑, These results suggest that ELF MF stimulation facilitates H2O2-dependent cell death in cancer cells as its effect was enhanced nearly two-fold
TumCD↑, 1 μM MTX
CellMemb↑,
eff↑, ELF-MF enhance the effects of methotrexate on THP-1 and PC12 cells

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

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
TumCG↓, Exposure to Thomas-EMF inhibited tumour growth in mice
Ca+2↑, exposure of malignant cells to Thomas-EMF for > 15 min promoted Ca2+ influx
selectivity↑, but did not effect non-malignant cells
*Ca+2∅, only malignant cells showed enhanced Ca2+ uptake following exposure to Thomas-EMF.
ROS↑, EMF-dependent increases in reactive oxygen species, rapid influx of Ca2+, or activation of specific signaling pathway
HSP70/HSPA5↑, Some studies have shown increased expression of HSP70, a marker of cellular stress responses, in response to EMF exposures
AntiCan↑, These observations suggest that the Thomas-EMF could provide a potential anti-cancer therapy.

527- MF,    Effects of Fifty-Hertz Electromagnetic Fields on Granulocytic Differentiation of ATRA-Treated Acute Promyelocytic Leukemia NB4 Cells
- in-vitro, AML, APL NB4
ROS↑, a significant increase in ROS levels was observed shortly after exposure to ELF-EMF
other↑, F-EMF exposure promotes ATRA-induced differentiation in APL NB4 cells and suggest the possible involvement of ROS and ERK signalling pathway in this phenomenon
p‑ERK↑, ERK1/2 phosphorylation
TumCP↓, ELF-EMF exposure decreases cellular proliferation potential

528- MF,  Caff,    Pulsed electromagnetic fields affect the intracellular calcium concentrations in human astrocytoma cells
- in-vitro, GBM, U373MG
Ca+2↑, After exposure to electromagnetic fields the basal [Ca(2+)](i) levels increased significantly from 143 +/- 46 nM to 278 +/- 125 nM
TumCP∅, Moreover the electromagnetic fields that affected [Ca(2+)](i) did not cause cell proliferation or cell death and the proliferation indexes remained unchanged after exposure.
TumCD∅,
eff↑, However, the [Ca 2+]i levels in normal and caffeine-treated cells were signicantly higher after EMF exposure than in sham exposed cells exposed cells

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
Ca+2↑, In both the KG-1 and HUVECs, PEMF stimulation resulted in enhanced Ca2+ influx
selectivity↑, response of [Ca2+]i due to PEMF stimulation appeared in the opposite direction in HUVECs.
*Inflam↓, PEMF also effected a decrease in the inflammatory cytokines TNF-alpha and NFkB in macrophage-like cells [9]. Although these studies suggest that PEMF is effective in wound healing and at attenuating inflammation
*TNF-α↓,
*NF-kB↓,
*Ca+2↓, ATP-sensitive Ca2+ influx and ER Ca2+ release of HUVECs were decreased by PEMP stimulation.

530- MF,    Low frequency sinusoidal electromagnetic fields promote the osteogenic differentiation of rat bone marrow mesenchymal stem cells by modulating miR-34b-5p/STAC2
- in-vivo, Nor, NA
*miR-34b-5p↓, expression of miR-34b-5p decreased under SEMF stimulation,
*ALP↑, significant upregulation in the relative expression levels of osteogenic markers (ALP, RUNX2, BMP2, OCN, and OPN)
*RUNX2↑,
*BMP2↑,
*OCN↑,
*OPN↑,
*β-catenin/ZEB1↑, protein expression levels of osteogenic makers, including Active-β-catenin, RUNX2, and ALP, were elevated upon SEMFs exposure at 0.4 mT, 0.7 mT, and 1 mT
*STAC2↑, subsequently increasing STAC2 level.
*Diff↑, electromagnetic fields promote the osteogenic differentiation
*BMD↑, low-frequency SEMFs promote osteogenesis

531- MF,    6-mT 0-120-Hz magnetic fields differentially affect cellular ATP levels
- in-vitro, Cerv, HeLa - in-vitro, CRC, HCT116 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, Nor, RPE-1 - in-vitro, Nor, GP-293
ATP⇅, variable effects

532- MF,    A 50 Hz magnetic field influences the viability of breast cancer cells 96 h after exposure
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
TumCP↓,
MMP↓, MCF-7 breast cancer cells showed a significant decrease in ΔΨM compared with control cells after 4 and 24 h of exposure only when ΔΨM was analyzed at 96 h
ROS↑, All three breast cell lines analyzed showed an increase in ROS levels compared to those in nonexposed cells after both 4 h and 24 h of 1.0 mT ELF-MF exposure
eff↝, short-term exposure (4–8 h, 0.1 mT and 1.0 mT) led to an increase in viability in breast cancer cells, while long and high exposure (24 h, 1.0 mT) led to a decrease in viability and proliferation in all cell lines.
selectivity↑, Conversely, we did not observe significant differences in MCF-10A live cell number after 0.1 mT ELF-MF cell exposure

533- MF,    Effects of extremely low-frequency magnetic fields on human MDA-MB-231 breast cancer cells: proteomic characterization
- in-vitro, BC, MDA-MB-231 - in-vitro, Nor, MCF10
TumCD↑,
necrosis↑, in normal MCF10A cells
mt-ROS↑, ELF-MF significantly increase the mitochondrial reactive oxygen species production in both MCF-10A and MDA-MB-231 cells, compared to the unexposed cell
other↑, ELF-MF exposed MCF-10A cells exhibited 53 upregulated and 189 downregulated proteins compared with control cells while exposed MDA-MB-231 cells showed 242 upregulated and 86 downregulated proteins compared with the control cells.
*STAT3↓, normal cells
STAT3↑, cancer cells

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
Ca+2↑, Exposure of the MDA-MB-231 cells to ELF-EMF also increased the fluorescence of the Ca2+ dye, FLUO-4 (AM) within 30 min, indicating an increase in Ca2+ influx compared to the control
Apoptosis↑,
eff↝, The cell viability increased with increases in the applied frequency. The ELF-EMF at 7.83Hz± 0.3 Hz showed the strongest inhibition of cell viability among the three frequency conditions
eff↑, The cells exposed to 6 h switching at 7.83Hz±0.3 Hz and 1mT for 2 consecutive days showed the strongest decrease in cell viability (from 100% to 40%)
selectivity↑, By contrast, the viability of the noncancerous M10 cells was unchanged by exposure to the T1 conditions,
eff↝, These differences in Ca2+ uptake behavior in the malignant cells could explain why MCF-7 and MDA-MB-231 cells are more sensitive than non-malignant M10 breast cells to EMF exposure.
eff↝, Our study also showed a clear window of vulnerability of cancer cells to ELF-EMF and that greater doses and magnitudes would be not unnecessarily better

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
Apoptosis↑,
miR-129-5p↑, A172 only
Ca+2↑,
eff↝, In contrast, the cervix cancer cell line and the prostate cancer cell line remained largely unaffected.

536- MF,    Comparison of pulsed and continuous electromagnetic field generated by WPT system on human dermal and neural cells
- in-vitro, Nor, SH-SY5Y - in-vitro, GBM, T98G - in-vitro, Nor, HDFa
other∅, did not show any negative effect of the generated EMF on either normal cells or tumor cell lines

537- MF,  immuno,    Integrating electromagnetic cancer stress with immunotherapy: a therapeutic paradigm
- Review, Var, NA
Apoptosis↑,
ROS↑,
TumAuto↑,
Ca+2↑, Ca++ ion tumor-cell entry
ATP↓, ATP depletion
eff↑, In physical terms, the rate of rise in a magnetic pulse or oscillation (i.e., its “sharpness”) is conveyed as dB/dt). The EMF induced by that particular period of rise to the maximum amplitude may be more impactful on unique tumor cellular features
eff↑, The induction intensity (dB/dt) may well be more critical than the field maximum amplitude (B max) in this setting

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

2257- MF,  HPT,    HSP70 Inhibition Synergistically Enhances the Effects of Magnetic Fluid Hyperthermia in Ovarian Cancer
- in-vitro, Ovarian, NA
eff↑, HSP70 inhibition combination with MFH generate a synergistic effect and could be a promising target to enhance MFH therapeutic outcomes in ovarian cancer.
eff↑, A significantly reduction in tumor growth rate was observed with combination therapy

2260- MF,    Alternative magnetic field exposure suppresses tumor growth via metabolic reprogramming
- in-vitro, GBM, U87MG - in-vitro, GBM, LN229 - in-vivo, NA, NA
TumCP↓, proliferation of human glioblastoma multiforme (GBM) cells (U87 and LN229) was inhibited upon exposure to AMF within a specific narrow frequency range, including around 227 kHz.
TumCG↓, daily exposure to AMF for 30 min over 21 days significantly suppressed tumor growth and prolonged overall survival
OS↑,
ROS↑, This effect was associated with heightened reactive oxygen species (ROS) production and increased manganese superoxide dismutase (MnSOD) expression.
SOD2↑,
eff↓, anti-cancer efficacy of AMF was diminished by either a mitochondrial complex IV inhibitor or a ROS scavenger.
ECAR↓, decrease in the extracellular acidification rate (ECAR) and an increase in the oxygen consumption rate (OCR).
OCR↑,
selectivity↑, This suggests that AMF-induced metabolic reprogramming occurs in GBM cells but not in normal cells. Furthermore, in cancer cells, AMF decreased ECAR and increased OCR, while there were no changes in normal cells.
*toxicity∅, did not affect non-cancerous human cells [normal human astrocyte (NHA), human cardiac fibroblast (HCF), human umbilical vein endothelial cells (HUVEC)].
TumVol↓, The results showed a significant treatment effect, as assessed by tumor volume, after conducting AMF treatment five times a week for 2 weeks
PGC-1α↑, Corresponding to the rise in ROS, there was also a time-dependent increase in PGC1α protein expression post-AMF exposure
OXPHOS↑, enhancing mitochondrial oxidative phosphorylation (OXPHOS), leading to increased ROS production
Glycolysis↓, metabolic mode of cancer cells to shift from glycolysis, characteristic of cancer cells, toward OXPHOS, which is more typical of normal cells.
PKM2↓, We extracted proteins that changed commonly in U87 and LN229 cells. Among the individual proteins related to metabolism, pyruvate kinase M2 (PKM2) was found to be inhibited in both.

2261- MF,    Tumor-specific inhibition with magnetic field
- in-vitro, Nor, GP-293 - in-vitro, Liver, HepG2 - in-vitro, Lung, A549
ROS↑, It enhances cell oxidative stress response and regulates apoptosis signaling pathway, changing intracellular Ca2+ concentration to induce apoptosis
Ca+2↓,
Apoptosis↑,
*selectivity↑, No signicant difference was found between the exposed 293T cell count versus the control group without magnetic exposure on the third day of exposure.
TumCG↓, Hepg2, A549 cell counts were signicantly lower than the unexposed control groups (the highest inhibition rate of Hepg2 was about 18%, and the highest inhibition rate of A549 was about 30%).
*i-Ca+2↓, Normal cells 293T showed a significant decrease in intracellular free calcium ion,
i-Ca+2↑, solid tumor cells showed no signicant change, while suspended tumor showed a slight increase in calcium ion

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
Apoptosis↑, Ding et al., 8 it was demonstrated that 24‐h exposure to 60 Hz, 5 mT ELF‐EMF could potentiate apoptosis induced by H2O2 in HL‐60 leukaemia cell lines.
H2O2↑,
ROS↑, One of the main mechanisms proposed for defining anticancer effects of ELF‐EMF is induction of apoptosis through upregulation of reactive oxygen species (ROS) which has also been confirmed by different experimental studies.
eff↑, intermittent 100 Hz, 0.7 mT EMF significantly enhanced rate of apoptosis in human hepatoma cell lines pretreated with low‐dose X‐ray radiation.
eff↑, 50 Hz, 45 ± 5 mT pulsed EMF, significantly potentiated rate of apoptosis induced by cyclophosphamide and colchicine
Ca+2↑, Over the past few years, lots of data have shown that ELF‐EMF exposure regulates intracellular Ca2+ level
MAPK↑, Mitogen‐activated protein kinase (MAPK) cascades are among the other important signalling cascades which are stimulated upon exposure to ELF‐EMF in several types of examined cells
*Catalase↑, ELF‐EMF exposure can upregulate expression of different antioxidant target genes including CAT, SOD1, SOD2, GPx1 and GPx4.
*SOD1↑,
*GPx1↑,
*GPx4↑,
*NRF2↑, Activation and upregulation of Nrf2 expression, the master redox‐sensing transcription factor may be the most prominent example in this regard which has been confirmed in a Huntington's disease‐like rat model.
TumAuto↑, Activation of autophagy, ER stress, heat‐shock response and sirtuin 3 expression are among the other identified cellular stress responses to ELF‐EMF exposure
ER Stress↑,
HSPs↑,
SIRT3↑,
ChemoSen↑, Contrarily, when chemotherapy and ELF‐EMF exposure are performed simultaneously, this increase in ROS levels potentiates the oxidative stress induced by chemotherapeutic agents
UPR↑, In consequence of ER stress, cells begin to initiate UPR to counteract stressful condition.
other↑, Since the only proven effects of ELF‐EMF exposure on cells are cellular adaptive responses, ROS overproduction and intracellular calcium overload
PI3K↓, figure 3
JNK↑,
p38↑,
eff↓, ontrarily, when cells are exposed to ELF‐EMF, a new source of ROS production is introduced in cells which can at least partially reverse anticancer effects observed with cell's treatment with melatonin.
*toxicity?, More importantly, ELF‐EMF exposure to normal cells in most cases has shown to be safe and un‐harmful.

3458- MF,    Magnetic Control of Protein Expression via Magneto-mechanical Actuation of ND-PEGylated Iron Oxide Nanocubes for Cell Therapy
- in-vitro, GBM, NA
ER Stress↑, Western blot studies indicated actuated, intracellular cubic ND-PEG-SPIONs can cause mild ER stress at short periods (up to 3 h) of postmagnetic field treatment thus leading to the unfolded protein response
UPR↑,
Ca+2↑, Studies have shown that applying low-frequency magnetic fields (50 Hz) to young rats leads to stimulation of Ca2+ channel transport and therefore increases intracellular Ca2+ levels.
TRAIL↓, n the present study, we observed a similar effect where MMA caused ER stress, which resulted in a decrease in TRAIL secretion in tC17.2 stem cells
GRP78/BiP↑, A slight expression increase was also noted for the other chaperone, GRP78, for all treatment conditions.

3459- MF,    EFFECT OF PULSED ELECTROMAGNETIC FIELDS ON ENDOPLASMIC RETICULUM STRESS
- in-vitro, Cerv, HeLa
GRP78/BiP↑, the expression of BiP, Grp94 and CHOP were increased in HeLa cells upon PEMF exposure.
GRP94↑,
CHOP↑,
ER Stress↓, Our main findings are that PEMF exposure (8 Hz and meant flux density of 0.56 mT) is able to reduce the elevated activity of ER stress markers induced by tunicamycin, in HepG2 cell line.

3462- MF,    The Effect of a Static Magnetic Field on microRNA in Relation to the Regulation of the Nrf2 Signaling Pathway in a Fibroblast Cell Line That Had Been Treated with Fluoride Ions
- in-vitro, Nor, NA
*NRF2↑, Moreover, the static magnetic field had a beneficial effect on the cells with fluoride-induced oxidative stress due to stimulating the antioxidant defense.
*Keap1↓, exposure to an SMF induced a significant reduction in the level of KEAP1 mRNA compared to the untreated cells
*SOD↑, also increased activity of the antioxidant enzymes (superoxide dismutase—SOD and glutathione peroxidase—GPx) compared to the cells that had only been treated with fluoride
*GPx↑,
*ROS↓, SMF resulted in a decrease in the production of intracellular ROS and a decrease in the MDA concentration, as was shown in our previous report
*MDA↓,
*SOD1↑, SOD1, SOD2 and GSR (glutathione reductase) a significant increase in their expression was revealed in the cells that had been co-exposed to fluoride and an SMF with a 0.65 T flux density
*SOD2↑,
*GSR↑,

3463- MF,    Pulsed Electromagnetic Fields Alleviates Hepatic Oxidative Stress and Lipids Accumulation in db/db mice
- in-vivo, NA, NA
*hepatoP↑, PEMF exposure could protect the liver from oxidative stress injury by decreasing MDA and GSSG level, promoting reduced GSH level, and increasing GSH-Px activity and expression in comparison with sham group
*MDA↓,
*GSSG↓,
*GSH↑,
*GPx↑,
*antiOx↑, PEMF could increase antioxidant enzymes activity and alleviate lipid accumulation in fatty liver.
*SREBP1↓, PEMF exposure ameliorated hepatic steatosis through reducing the expression of SREBP-1c to regulate the lipid synthesis.

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


Showing Research Papers: 1 to 50 of 262
Page 1 of 6 NOTCH&page=2&exSp=open">Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 262

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   Fenton↑, 1,   Ferroptosis↑, 1,   GPx1↓, 1,   GPx1↑, 1,   GPx4↓, 1,   GSR↑, 1,   H2O2↑, 2,   Iron↑, 1,   MDA↑, 1,   OXPHOS↑, 2,   ROS↑, 17,   ROS↝, 1,   mt-ROS↑, 1,   RPM↑, 3,   SIRT3↑, 1,   SOD↓, 1,   SOD↑, 2,   SOD1↓, 1,   SOD1↑, 1,   SOD2↓, 1,   SOD2↑, 2,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   ATP↑, 1,   ATP⇅, 1,   mitResp↑, 1,   MMP↓, 2,   MMP↑, 1,   OCR↑, 1,   PGC-1α↑, 1,  

Core Metabolism/Glycolysis ⓘ

ECAR↓, 1,   Glycolysis↓, 1,   PKM2↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 9,   BAX↑, 1,   Bcl-2↓, 3,   Casp↑, 1,   Casp3↑, 3,   Casp7↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Endon↑, 1,   Ferroptosis↑, 1,   iNOS↑, 2,   JNK↑, 1,   MAPK↑, 2,   necrosis↑, 1,   p38↑, 1,   TRAIL↓, 1,   TRPV1↑, 1,   TumCD↑, 3,   TumCD∅, 1,  

Transcription & Epigenetics ⓘ

miR-129-5p↑, 1,   other↓, 3,   other↑, 4,   other∅, 1,   tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↓, 1,   ER Stress↑, 3,   GRP78/BiP↑, 2,   GRP94↑, 1,   HSP70/HSPA5↓, 1,   HSP70/HSPA5↑, 2,   HSP90↓, 1,   HSPs↑, 1,   UPR↑, 2,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   TumAuto↑, 4,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 5,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   p‑ERK↑, 1,   miR-125b↓, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↑, 1,   p‑STAT3↑, 1,   TumCG↓, 6,  

Migration ⓘ

Ca+2↓, 1,   Ca+2↑, 14,   Ca+2↝, 1,   i-Ca+2↑, 1,   MMP2↑, 1,   TumCMig↓, 1,   TumCP↓, 5,   TumCP∅, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   EPR↑, 1,   VEGFR2↓, 2,  

Barriers & Transport ⓘ

CellMemb↑, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,   NF-kB↑, 2,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   Dose?, 1,   Dose∅, 1,   eff↓, 2,   eff↑, 13,   eff↝, 6,   selectivity↑, 7,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   OS↑, 2,   QoL↑, 1,   TumVol↓, 2,  
Total Targets: 111

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 2,   GPx1↑, 2,   GPx4↑, 2,   GSH↑, 1,   GSR↑, 1,   GSSG↓, 1,   Keap1↓, 1,   MDA↓, 2,   NRF2↑, 2,   OXPHOS↓, 1,   ROS↓, 3,   ROS↑, 1,   ROS↝, 1,   RPM↑, 1,   SOD↑, 2,   SOD1↑, 2,   SOD2↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↝, 1,   MMP∅, 1,   MPT↑, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↑, 1,   HK2↑, 1,   PFKL↑, 1,   PFKM↑, 1,   PFKP↑, 1,   PKM2↑, 1,   SREBP1↓, 1,  

Cell Death ⓘ

BAX↓, 1,   Bcl-2∅, 1,   BMP2↑, 1,   Cyt‑c↑, 1,  

Kinase & Signal Transduction ⓘ

OCN↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   p‑GSK‐3β↑, 1,   RUNX2↑, 1,   STAT3↓, 1,  

Migration ⓘ

Ca+2↓, 2,   Ca+2∅, 1,   i-Ca+2↓, 1,   OPN↑, 1,   STAC2↑, 1,   β-catenin/ZEB1↑, 1,  

Angiogenesis & Vasculature ⓘ

angioG↑, 2,   miR-34b-5p↓, 1,  

Barriers & Transport ⓘ

GLUT1↑, 1,   GLUT4↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioEnh↑, 4,   eff↓, 2,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

ALP↑, 1,   BMD↑, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   toxicity?, 1,   toxicity∅, 1,  
Total Targets: 59

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:%  Cells:%  prod#:172  Target#:%  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page