Magnetic Fields Cancer Research Results

MF, Magnetic Fields: Click to Expand ⟱
Features: Therapy

Magnetic Fields — externally applied static or time-varying magnetic fields used to alter cellular signaling, redox state, ion handling, membrane behavior, metabolism, or neural activity without introducing a chemical agent. They are a physical therapeutic modality and include static magnetic fields (SMF), extremely-low-frequency magnetic fields (ELF-MF), pulsed electromagnetic fields (PEMF), and other non-rotating oscillating/time-varying magnetic fields. Common abbreviations include MF, SMF, ELF-MF, EMF, and PEMF. Biological effects are strongly dependent on field strength, frequency, waveform, gradient, duty cycle, exposure duration, and tissue or cell type. Rotating magnetic fields are excluded here because they are represented separately as pid 192; magnetic-nanoparticle-dependent magnetothermal or magnetomechanical effects are also better assigned primarily to the magnetic nanoparticle product.

Primary mechanisms (ranked):

  1. Redox modulation and ROS perturbation, including radical-pair and mitochondrial mechanisms; cancer cells may develop sustained oxidative stress whereas normal cells frequently show adaptive antioxidant responses.
  2. Ca²⁺ and ion-channel modulation, particularly TRPC, voltage-gated channels, intracellular Ca²⁺ handling, and ER–mitochondrial Ca²⁺ communication.
  3. Mitochondrial and bioenergetic modulation, including membrane potential, electron transport, ATP production, mitochondrial permeability, and metabolic reprogramming.
  4. Cell proliferation, cell-cycle, apoptosis, and senescence signaling through pathways including EGFR/PI3K/AKT/mTOR, MAPK/ERK, caspases, PARP, Bax and survivin.
  5. Membrane permeability and drug-uptake modulation, producing context-dependent chemosensitization to agents including doxorubicin, etoposide and methotrexate.
  6. Inflammatory and stress-response modulation including NF-κB, cytokine signaling, HSPs, ER stress and adaptive antioxidant pathways.
  7. Migration, invasion, angiogenesis and tumor-microenvironment modulation; effects are field-parameter and tumor-model dependent.

Bioavailability / PK relevance: Conventional pharmacokinetic concepts do not apply because the intervention is a physical field rather than an absorbed drug. Relevant exposure variables are magnetic flux density, field gradient, frequency, waveform, pulse width, repetition rate, duty cycle, spatial distribution, treatment duration and tissue depth. Magnetic fields can penetrate tissue without the concentration gradients characteristic of drugs, but induced electric fields and biological coupling vary markedly with geometry and frequency.

In-vitro vs systemic exposure relevance: Effects are not concentration-driven. Many experimental results cannot be generalized between devices because apparently small differences in waveform, frequency, flux density, orientation, gradient and exposure duration can change the biological response. Static fields ranging from millitesla to tesla and PEMF/ELF protocols ranging from weak fields to substantially stronger stimulation should therefore be treated as distinct exposure regimens rather than as a single dose-response continuum.

Clinical evidence status: Cancer treatment remains predominantly preclinical, with cell-culture and animal evidence plus limited supportive or adjunctive human use. Evidence supports parameter-dependent anticancer effects and chemosensitization, but non-rotating magnetic-field exposure alone is not an established standard anticancer therapy. PEMF has established clinical use in several musculoskeletal applications and has been studied as supportive therapy in oncology. Repetitive transcranial magnetic stimulation has substantially stronger human evidence in neurological and psychiatric applications, including investigational use in Alzheimer’s disease, but should not be interpreted as evidence that generic magnetic-field exposure is an established systemic cancer treatment.

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">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

Magnetic Field Mechanisms in Cancer

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 ROS and redox homeostasis ↑ ROS (context-dependent); ↑ oxidative stress ↑ transient ROS followed by ↔ or ↓ ROS in adaptive protocols P, R, G Redox perturbation One of the most recurrent MF mechanisms. Direction is strongly field- and cell-dependent; sustained ROS elevation is reported in several cancer models and during chemotherapy sensitization.
2 Ca²⁺ and ion-channel signaling ↑ Ca²⁺ signaling or dysregulation; altered TRPC and voltage-sensitive channel activity ↑ transient signaling with homeostatic recovery (context-dependent) P, R Electrophysiological signal transduction Ca²⁺ is a major mechanistic bridge between membrane sensing, mitochondria, ROS, proliferation and apoptosis. Response depends strongly on waveform and frequency.
3 Mitochondrial function and membrane potential ↓ ΔΨm; altered respiration; ↑ mitochondrial stress ↔ or reversible modulation (context-dependent) P, R, G Bioenergetic destabilization Mitochondrial effects can arise downstream of ROS and Ca²⁺ signaling and contribute to apoptotic commitment.
4 Apoptosis and caspase signaling ↑ apoptosis; ↑ caspases; ↑ PARP cleavage; ↑ Bax; ↓ survivin ↔ or substantially weaker response in selective protocols R, G Programmed cell death Reported with several PEMF and time-varying field protocols and can be amplified when combined with chemotherapy.
5 EGFR PI3K AKT mTOR signaling ↓ EGFR/AKT/mTOR signaling (model-dependent) ↔ or mixed R, G Growth-signal suppression Particularly supported in static-field experiments; response varies with cell type, cell density and field intensity.
6 Cell cycle and proliferation ↓ proliferation; ↑ cell-cycle arrest or mitotic disruption ↔ or mixed G Growth suppression Effects are highly protocol-specific. Some exposures are neutral or can stimulate proliferation, so suppression should not be treated as universal.
7 DNA damage and DNA-damage response ↑ DNA damage; ↑ ATM/p53/p21 signaling (context-dependent) ↔ or mixed; protective responses reported with some protocols R, G Genotoxic stress and repair modulation Often secondary to ROS and particularly evident during combination treatment with chemotherapy or radiation. Magnetic fields alone are not consistently genotoxic, and some static-field protocols can reduce radiation-associated DNA damage.
8 Chemosensitization and drug uptake ↑ chemotherapy response; ↑ drug uptake or cytotoxicity ↔ or ↑ toxicity (drug-dependent) R, G Adjunctive anticancer effect Documented with doxorubicin, etoposide and other agents. Selectivity is not guaranteed; normal-cell toxicity must be evaluated for each field-drug combination.
9 Glutathione and antioxidant buffering ↓ GSH reserve or altered GSH/GSSG balance (context-dependent) ↑ GSH or antioxidant adaptation in some protocols R, G Redox buffering modulation GSH depletion is best interpreted as a consequence of oxidative load rather than a universal direct MF target.
10 NRF2 antioxidant response ↔ / mixed; inadequate adaptive response in some oxidative protocols ↑ NRF2 and antioxidant-response signaling in some protective protocols R, G Adaptive antioxidant defense NRF2 direction is not uniform enough to classify MF globally as either an NRF2 activator or inhibitor.
11 ER stress and unfolded protein response ↑ ER stress and UPR (model-dependent) ↑ adaptive stress response or ↔ R, G Proteostasis stress Can develop secondary to ROS, altered Ca²⁺ handling and mitochondrial dysfunction.
12 Mitochondrial permeability transition ↑ MPTP opening propensity ↔ or reversible opening R Mitochondrial death commitment Supported mechanistically for specific ELF-MF exposures through ROS-sensitive pathways; should not be generalized to all magnetic fields.
13 Glycolysis and cellular energetics ↓ glycolytic flux or altered ATP production (model-dependent) ↔ or metabolic adaptation R, G Metabolic reprogramming Some frequency-tuned exposures suppress glycolysis, but this is substantially less universal than ROS or Ca²⁺ modulation.
14 HIF-1α and angiogenic signaling ↓ HIF-1α / VEGF in selected models ↑ VEGF or tissue-repair signaling in some regenerative protocols G Angiogenesis modulation Potential cancer-versus-normal-tissue divergence is attractive but remains highly exposure- and model-specific.
15 NF-κB and inflammatory signaling ↓ NF-κB and inflammatory signaling in selected models ↓ inflammatory cytokines in many regenerative PEMF applications R, G Inflammation modulation Better established as an anti-inflammatory/regenerative PEMF effect than as a universal cancer-cell mechanism.
16 Migration invasion and angiogenesis ↓ migration; ↓ invasion; ↓ angiogenic signaling in selected models ↔ or pro-repair angiogenesis (context-dependent) G Metastatic phenotype modulation Direction varies substantially with field protocol and normal-versus-tumor context.
17 Radiosensitization ↑ radiation-induced ROS and DNA damage in selected protocols Mixed; radioprotection has also been reported with other protocols R, G Modification of radiation response Both radiosensitizing and radioprotective responses have been reported; field parameters and tissue context determine direction.
18 Clinical Translation Constraint Field-specific response; substantial tumor heterogeneity Potential tissue-specific physiological effects G Translation limitation No pharmacokinetic dose metric exists. Field strength, frequency, waveform, geometry, gradients, duration and induced electric fields must be specified. Most anticancer evidence remains preclinical and protocols are poorly standardized.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr

MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure.




Alzheimer’s disease relevance: Repetitive transcranial magnetic stimulation (rTMS) is a non-invasive magnetic neuromodulation modality with randomized human evidence for modest improvement in global cognition in mild cognitive impairment and Alzheimer’s disease. The strongest recent evidence supports excitatory stimulation of cortical cognitive-network regions, particularly the dorsolateral prefrontal cortex. The mechanism is principally neural-network and synaptic modulation rather than the systemic ROS-based mechanism often discussed for low-intensity PEMF. Meta-analyses generally report cognitive benefit, but protocol heterogeneity, small trials and uncertain durability remain important limitations. rTMS should therefore be classified as investigational or adjunctive for AD rather than an established disease-modifying treatment.

Clinical evidence status: Multiple RCTs and meta-analyses support a modest short-term cognitive signal. Longer-term benefit remains less certain, optimal frequency/intensity/site protocols are not standardized, and evidence does not establish prevention or reversal of Alzheimer pathology.

Magnetic Stimulation in Alzheimer’s Disease

Rank Pathway / Axis Modulation TSF Primary Effect Notes / Interpretation
1 Cortical network excitability ↑ P, R Neuromodulation High-frequency rTMS and excitatory stimulation of cortical network hubs can increase cortical responsiveness.
2 Synaptic plasticity ↑ R, G Plasticity enhancement Repeated stimulation can produce LTP-like network effects and is a leading explanation for persistence beyond the stimulation session.
3 Cognitive-network connectivity ↑ G Network normalization DLPFC and related cortical networks are the most consistently studied targets.
4 Global cognition ↑ G Clinical cognitive improvement Recent meta-analyses show modest improvement in MMSE, MoCA or ADAS-Cog outcomes, although heterogeneity remains substantial.
5 Neuroinflammation and neurotrophic signaling ↓ inflammation; ↑ neurotrophic signaling (context-dependent) G Secondary neurobiological effects Supported mainly by mechanistic and preclinical studies; less directly established than cortical-network effects in human AD.
6 Clinical Translation Constraint ↔ G Protocol heterogeneity Optimal stimulation site, frequency, intensity, pulse count, session number and maintenance schedule remain unresolved; long-term disease modification has not been demonstrated.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr
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, MCF7 - 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/ATG6↑,
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, MCF7
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

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

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

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

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↓,

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.

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↑,

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

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.

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.

2238- MF,    Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects
- Review, Var, NA
*BMD↑, Therapeutic bone-growth stimulation via Ca2+/nitric oxide/cGMP/protein kinase G. Multiple studies have implicated increased Ca2+ and nitric oxide in the EMF stimulation of bone growth
*VGCC↑, increased VGCC activity following EMF exposure and suggests, therefore, that VGCC stimulation in the plasma membrane is directly produced by EMF exposure.
*Ca+2↑, Other studies, each involving VGCCs, summarized in Table 1, also showed rapid Ca2+ increases following EMF exposure [8, 16, 17, 19, 21].
*NO↑, Multiple studies have implicated increased Ca2+ and nitric oxide in the EMF stimulation of bone growth
*eff↓, Voltage-gated calcium channel stimulation leads to increased intracellular Ca2+, which can act in turn to stimulate the two calcium/calmodulin-dependent nitric oxide synthases and increase nitric oxide.

2239- MF,    Time-varying magnetic fields increase cytosolic free Ca2+ in HL-60 cells
- in-vitro, AML, HL-60
Ca+2↑, cells exposed to only the time-varying magnetic field had a mean [Ca2+]i that was 34 +/- 10 nM (P less than 0.01, n = 11) higher than parallel control samples.
eff↝, Separate exposure to the radio-frequency (6.25 MHz) or static field (0.15 T) had no detectable effects.

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
*Ca+2↑, intracellular [Ca2+]i in C3H10T1/2 cells can be upregulated upon exposure to PEMF
*Diff↑, PEMF-induced C3H10T1/2 cell differentiation was Ca2+-dependent.
*BMD↑, pro-osteogenic effect of PEMF on Ca2+-dependent osteoblast differentiation
*Wnt↑, PEMF promoted the gene expression and protein synthesis of the Wnt/β-catenin pathway.
*β-catenin/ZEB1↑, PEMF activates the Wnt/b-catenin signaling pathway in C3H10T1/2 cells
*eff↝, These data indicated that increased intranuclear [Ca2+]i resulted in altered electrical activity in the nucleus.

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

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

522- MF,    Low Magnetic Field Exposure Alters Prostate Cancer Cell Properties
- in-vitro, Pca, PC3
MMP2↑, The 4 h LMF exposure caused a significant increase in MMP2 and MMP9, as well as in onco-miRs miR-155, miR-210, miR-21
MMP9↑,
miR-21↑,
miR-155↑, 57x
miR-210↑,
miR-200c↓, 1.25 fold decrease
miR-126↓, 2.5-fold decrease

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/KDR/Flk1↓,
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, MCF7 - 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

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

2242- MF,    Electromagnetic stimulation increases mitochondrial function in osteogenic cells and promotes bone fracture repair
- in-vitro, Nor, NA
*MMP↑, we show that application of a low intensity constant EM field source on osteogenic cells in vitro resulted in increased mitochondrial membrane potential and respiratory complex I activity and induced osteogenic differentiation.
*Diff↑,
*OXPHOS↑, effect was mediated via increased OxPhos activity
*BMD↑, EM field source enhanced fracture repair via improved biomechanical properties and increased callus bone mineralization
ATP∅, higher mitochondrial OxPhos activity leads to higher ATP production, increased cellular activity leads to increased ATP consumption.

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, MCF7 - 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, MCF7 - 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, MCF7 - 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

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/PTGS2↓,
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

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.

3471- MF,    The prevention effect of pulsed electromagnetic fields treatment on senile osteoporosis in vivo via improving the inflammatory bone microenvironment
- in-vivo, Nor, NA
*BMD↑, PEMF increased the bone mineral density of the proximal femur and L5 vertebral body and improved parameters of the proximal tibia and L4 vertebral body.
*NLRP3↓, PEMF also dramatically inhibited NLRP3-mediated low-grade inflammation in the bone marrow,
*proCasp1↓, PEMF inhibited the levels of NLRP3, proCaspase1, cleaved Caspase1, IL-1β, and GSDMD-N.
*cl‑Casp1↓,
*IL1β↓,
*GSDMD↓,

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/SREBF1↓, 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/KDR/Flk1↓, reducing the expression and activation levels of VEGFR2
P-gp/ABCB1↓, 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

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

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↑,

3468- MF,    An integrative review of pulsed electromagnetic field therapy (PEMF) and wound healing
- Review, NA, NA
*other↑, studies suggest that PEMF accelerates early stages of wound closure
*necrosis↓, By preventing necrosis, PEMF can potentially be used to reduce the incidence of ulcer formation and amputation in patients with diabetes.
*IL6↑, When gingival wounds were exposed to PEMF, one study measured an increased expression of various signalling molecules involved in proliferation including IL‑6, TGF‑β and iNOS
*TGF-β↑,
*iNOS↑,
*MMP2↑, The same study also found increased levels of MMP‑2, MCP‑1 and HO‑1 expression, all of which are thought to increase wound repair rate
*MCP1/CCL2↑,
*HO-1↑,
*Inflam↓, PEMF has also been shown to reduce inflammation in chronic wounds through both intracellular and extracellular effects.
*IL1β↓, Multiple studies have measured reductions in inflammatory cytokines (IL‑1β, IL‑6, TNF‑α) following PEMF treatment
*IL6↓,
*TNF-α↓,
*BioAv↑, Electrochemotherapy mediated by PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models
eff⇅, PEMF at 50Hz, 1mT for 1 hour had increased keratinocyte proliferation compared to control groups, while the same tissue exposed to PEMF at 60Hz, 1.5mT for 144 hours had reduced cell proliferation
DNAdam↑, At higher frequencies (6–7mT), an increase in DNA double-strand breaks, apoptosis and levels of reactive oxygen species (ROS) were measured, contributing to the inhibition of cell proliferation.
Apoptosis↑,
ROS↑,
TumCP↓,
*ROS↓, tissues exposed to lower frequencies of PEMF (1mT) had decreased ROS levels
*FGF↑, Furthermore, both diabetes-related and non-diabetes-related incision wounds had similar levels of increased FGF‑2, promoting angiogenesis and preventing necrosis in response to ischaemic injury

3469- MF,    Pulsed Electromagnetic Fields (PEMF)—Physiological Response and Its Potential in Trauma Treatment
- Review, NA, NA
*eff↑, According to this analysis, pulse repetition frequencies higher than 100 Hz with magnet flux densities between 1 mT and 10 mT lead to the highest presence of a cellular response, although this may vary depending on the cell type and stage of growth
*eff↝, Also, repeated applications over a prolonged period of more than 10 days show a higher effect than shorter periods, while a prolonged acute exposure lasting more than 24 h seems to be less effective than an acute exposure with less than 24 h applicat
*other↑, release of Ca2+ ion and the direct activation of PEMF on voltage-gated calcium channels (VGCCs) is of great relevance.
Ca+2↑, PEMF stimulation also leads to similar membrane effects, resulting in a Ca2+ influx, which triggers further cellular signals
ROS↑, It has been proposed that the accumulation of ROS or oxidative stress may cause the upregulation of heat shock proteins (Hsp70, HIF-1), leading to cell damage.
HSP70/HSPA5↑,
*NOTCH↑, PEMF has been shown to increase the expressions of Notch4 and Hey1 during osteogenic differentiation of MSCs, suggesting that the Notch pathway, important in cellular fate and bone development, is activated by PEMF in stem cells
*HEY1↑,
*p38↑, PEMF-induced osteogenic differentiation MSCs, as well as the activation of p38 MAPK
*MAPK↑,

3470- MF,    Pulsed electromagnetic fields inhibit IL-37 to alleviate CD8+ T cell dysfunction and suppress cervical cancer progression
- in-vitro, Cerv, HeLa
TNF-α↑, PEMF treatment significantly inhibited IL-37 expression (p < 0.05), promoted inflammatory factor release (TNF-α and IL-6), and activated oxidative stress, leading to increased CC cell apoptosis
IL6↑,
ROS↑,
Apoptosis↑,
TumCP↓, Co-culture of Hela cells with CD8+ T cells under PEMF treatment showed reduced proliferation (by 40%), migration, and invasion (p < 0.05).
TumCMig↓,
TumCI↓,


Showing Research Papers: 1 to 50 of 278
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 278

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

compII↓, 1,   K+↑, 1,   NA↑, 1,   PV↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

ATF3↑, 1,   Catalase↓, 1,   Catalase↑, 4,   Fenton↑, 1,   Ferroptosis↑, 2,   GPx↓, 1,   GPx1↓, 1,   GPx1↑, 1,   GPx4↓, 1,   GSH↓, 2,   GSH↑, 1,   GSH/GSSG↓, 2,   GSR↑, 1,   H2O2↑, 7,   mt-H2O2↑, 1,   Iron↓, 1,   Iron↑, 2,   i-Iron↓, 1,   lipid-P↑, 2,   MDA↑, 3,   OXPHOS↑, 3,   PARK2↑, 1,   Prx6↑, 1,   ROS↓, 2,   ROS↑, 55,   ROS⇅, 1,   ROS↝, 3,   mt-ROS↑, 2,   RPM↓, 1,   RPM↑, 6,   SIRT3↑, 1,   SOD↓, 3,   SOD↑, 2,   SOD1↓, 1,   SOD1↑, 1,   SOD2↓, 1,   SOD2↑, 2,   Thiols↓, 1,   xCT/SLC7A11↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

Ferritin↓, 1,   TfR1/CD71↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 2,   ATP↓, 2,   ATP↑, 2,   ATP⇅, 1,   ATP∅, 1,   ETC↓, 5,   mitResp↓, 1,   mitResp↑, 1,   MMP?, 1,   MMP↓, 10,   MMP↑, 1,   MPT↑, 2,   mtDam↑, 3,   OCR↓, 1,   OCR↑, 1,   PGC-1α↑, 1,   PINK1↑, 1,   PleEff↓, 1,   SDH↓, 2,   UCP1↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACAA1↓, 1,   ALAT↓, 2,   BCAP↓, 1,   cAMP⇅, 1,   cMyc↓, 2,   DHCR24↑, 1,   ECAR↓, 1,   FABP4↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   Glycolysis∅, 1,   lactateProd↑, 1,   PCK1↓, 1,   PKM2↓, 1,   PLIN1↓, 1,   PPARγ↑, 1,   Pyruv↓, 2,   SIRT1↑, 1,   TCA?, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 5,   p‑Akt↓, 2,   Apoptosis↑, 42,   p‑BAD↓, 1,   Bak↑, 1,   BAX↑, 5,   Bax:Bcl2↑, 1,   Bcl-2↓, 5,   Casp↑, 1,   Casp↝, 1,   Casp3↓, 1,   Casp3↑, 9,   cl‑Casp3↑, 2,   Casp7↓, 1,   Casp7↑, 3,   cl‑Casp7↑, 1,   Casp8↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 3,   cl‑Casp9↑, 1,   Chk2↑, 2,   Cyt‑c↑, 3,   Cyt‑c↝, 1,   Endon↑, 1,   Fas↑, 1,   Ferroptosis↑, 2,   iNOS↑, 2,   JNK↑, 1,   lysoMP↓, 2,   lysoMP↑, 3,   MAPK↓, 1,   MAPK↑, 3,   Mcl-1↓, 1,   Necroptosis↑, 1,   necrosis↑, 1,   p38↑, 3,   survivin↓, 3,   Telomerase↓, 2,   TRPV1↑, 1,   TRPV1↝, 1,   TumCD↑, 11,   TumCD∅, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

BowelM↑, 2,   ChrMod↑, 2,   p‑H3↓, 1,   miR-129-5p↑, 1,   miR-21↑, 1,   other↓, 3,   other↑, 7,   other↝, 3,   other∅, 1,   tumCV↓, 8,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   ER Stress↓, 1,   ER Stress↑, 3,   GRP78/BiP↑, 1,   GRP94↑, 1,   HSP70/HSPA5↓, 2,   HSP70/HSPA5↑, 7,   HSP70/HSPA5∅, 1,   HSP90↓, 2,   HSPs↑, 1,   HSPs∅, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

ATG5↑, 1,   Beclin-1/ATG6↑, 2,   LC3II↑, 1,   MitoP↑, 1,   p62↑, 1,   TumAuto↑, 6,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   p‑CHK1↓, 1,   DNAdam↑, 14,   P53↑, 9,   P53↝, 1,   cl‑PARP↑, 3,   γH2AX↑, 1,   p‑γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1?, 1,   CDK1↓, 1,   p‑CDK2↓, 1,   CycB/CCNB1↓, 2,   cycE/CCNE↓, 1,   E2Fs↓, 1,   mitA↑, 1,   P21↑, 2,   PLK1↓, 1,   TumCCA↑, 16,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD133↓, 2,   CD44↓, 2,   CSCs↓, 2,   Diff↑, 1,   EMT↓, 1,   ERK↑, 1,   p‑ERK↑, 2,   p‑ERK↝, 1,   GSK‐3β↑, 1,   miR-125b↓, 1,   miR-34a↑, 1,   mTOR↓, 2,   Nanog↓, 2,   PI3K↓, 2,   PTEN↓, 1,   RAS↑, 1,   SOX2↓, 2,   STAT3↑, 1,   p‑STAT3↑, 1,   TOP2↑, 1,   TumCG↓, 26,   VGCC↑, 1,   VGSC↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 2,   Ca+2↑, 29,   Ca+2↝, 3,   i-Ca+2↑, 1,   CAFs/TAFs↓, 1,   Cartilage↑, 1,   CCDC150↓, 1,   COL4↓, 1,   CXCL12↓, 1,   F-actin↓, 1,   FOSB↑, 1,   ITGA1∅, 1,   ITGA11↓, 1,   ITGA5∅, 1,   ITGB1∅, 1,   ITGB3∅, 1,   ITGB4∅, 1,   LAMB3↑, 1,   miR-155↑, 1,   miR-200c↓, 1,   miR-486↑, 1,   MMP1↑, 1,   MMP2↓, 1,   MMP2↑, 2,   MMP2∅, 1,   MMP3↑, 1,   MMP9↓, 1,   MMP9↑, 1,   MMP9∅, 1,   MMPs↓, 1,   Na+↑, 1,   Rho↓, 1,   Slug↓, 1,   p‑SMAD2↓, 1,   SMAD3↓, 1,   p‑SMAD3↓, 1,   TGF-β↓, 2,   THBS2↓, 1,   TRPC1↑, 1,   TumCI↓, 7,   TumCMig↓, 9,   TumCP↓, 22,   TumCP∅, 1,   TumMeta↓, 7,   Twist↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 8,   angioG↑, 1,   ECM/TCF↓, 1,   EGFR↓, 1,   EGFR↝, 1,   p‑EGFR↓, 1,   EPR↑, 2,   Hif1a↓, 1,   miR-126↓, 1,   miR-210↑, 1,   NO↑, 1,   nucleolin↑, 1,   VEGF↓, 2,   VEGF↑, 1,   VEGFR2/KDR/Flk1↓, 2,  

Barriers & Transport(tgid=15) ⓘ

CellMemb↑, 10,   Na+↑, 1,   P-gp/ABCB1↓, 3,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↓, 1,   CD4+↑, 3,   COX2/PTGS2↓, 1,   CXCc↓, 1,   CXCL9↓, 1,   DCells↑, 3,   FOXP3↓, 1,   GM-CSF↓, 1,   IFN-γ↓, 1,   IL1↑, 1,   IL10↑, 2,   IL12↑, 1,   IL17↓, 2,   IL22↓, 1,   IL23↓, 1,   IL28↓, 1,   IL6↓, 2,   IL6↑, 1,   IL9↓, 1,   Imm↑, 2,   Imm↝, 1,   Inflam↓, 1,   LIF↑, 1,   Macrophages↑, 1,   NF-kB↓, 1,   NF-kB↑, 2,   PD-L1↑, 1,   RANTES↓, 1,   T-Cell↑, 1,   TNF-α↓, 2,   TNF-α↑, 2,  

Cellular Microenvironment(tgid=17) ⓘ

pH↓, 1,   i-pH↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   ChemoSen↑, 17,   ChemoSen∅, 1,   Dose?, 1,   Dose↓, 1,   Dose↑, 1,   Dose↝, 21,   Dose∅, 1,   eff↓, 14,   eff↑, 31,   eff⇅, 1,   eff↝, 15,   MDR1↓, 1,   RadioS↑, 6,   selectivity↑, 29,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 1,   BloodF↑, 1,   BMD↑, 2,   BMPs↑, 1,   Calcium↑, 1,   EGFR↓, 1,   EGFR↝, 1,   p‑EGFR↓, 1,   Ferritin↓, 1,   IL6↓, 2,   IL6↑, 1,   PD-L1↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   AntiTum↑, 1,   Appetite↑, 2,   breath↑, 2,   chemoP↑, 2,   ChemoSideEff↓, 1,   cognitive↑, 2,   hepatoP↑, 1,   OS↑, 16,   OS⇅, 1,   Pain↓, 6,   QoL↑, 3,   radioP↑, 3,   Sleep↑, 3,   Strength↑, 4,   toxicity↓, 1,   TumVol↓, 16,   Weight↑, 2,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,   CD8+↓, 1,   CD8+↑, 3,  
Total Targets: 343

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

PV↓, 3,   UFR↑, 2,   UR↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 9,   Catalase↑, 8,   GPx↑, 4,   GPx∅, 1,   GPx1↑, 5,   GPx3↑, 1,   GPx4↑, 5,   GSH↑, 1,   GSH∅, 1,   GSR↑, 3,   GSSG↓, 1,   HO-1↑, 1,   Iron↑, 1,   Keap1↓, 1,   MDA↓, 5,   MDA↑, 1,   NRF2↑, 3,   OXPHOS↓, 2,   OXPHOS↑, 2,   ROMO1↑, 1,   ROS↓, 28,   ROS↑, 8,   ROS⇅, 2,   ROS↝, 1,   ROS∅, 1,   mt-ROS↑, 2,   RPM↑, 1,   SOD↑, 9,   SOD1↑, 5,   SOD2↓, 1,   SOD2↑, 5,   TAC↑, 1,   Trx↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ADP:ATP↓, 1,   ATP↑, 3,   ETC↓, 2,   Insulin↓, 1,   mitResp↓, 1,   MMP↑, 3,   MMP⇅, 1,   MMP↝, 1,   MMP∅, 1,   MPT↑, 1,   OCR↑, 1,   mt-OCR↑, 1,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   cAMP↑, 2,   p‑CREB↑, 1,   ECAR↓, 1,   ECAR↑, 1,   FABP4↓, 1,   FAO↓, 1,   FAO↑, 1,   Glycolysis↓, 1,   Glycolysis↑, 2,   HK2↑, 2,   lactateProd↓, 1,   LDH↓, 1,   LDHB↑, 1,   NAD↑, 1,   PFKL↑, 2,   PFKM↑, 2,   PFKP↑, 1,   PKM2↑, 2,   PONs↓, 1,   PPARγ↓, 1,   PPP↓, 1,   SREBP1/SREBF1↓, 1,   TCA↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Akt↑, 2,   p‑Akt↓, 1,   p‑Akt↑, 1,   Apoptosis↓, 6,   BAD↓, 1,   BAX↓, 3,   Bcl-2↑, 1,   Bcl-2∅, 1,   Bcl-xL↑, 1,   BMP2↑, 2,   Casp1↓, 1,   cl‑Casp1↓, 1,   proCasp1↓, 1,   Casp3↓, 2,   Cyt‑c↑, 2,   GSDMD?, 1,   GSDMD↓, 1,   HEY1↑, 1,   HGF/c-Met↑, 1,   iNOS↓, 3,   iNOS↑, 1,   p‑JNK↓, 1,   p‑JNK↑, 3,   MAPK↓, 1,   MAPK↑, 2,   necrosis↓, 1,   p38↑, 2,   p‑p38↓, 1,   RKIP↑, 1,   YAP/TEAD↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

OCN↑, 1,   OCN∅, 1,   SOX9↑, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,   other?, 3,   other↓, 2,   other↑, 15,   other↝, 10,   TREM-1↓, 1,   tumCV↑, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 1,   HSP70/HSPA5↑, 5,   HSPs↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

E2Fs↑, 1,   P21↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ALDH↑, 1,   cFos↑, 1,   Diff↓, 1,   Diff↑, 9,   Diff↝, 1,   ERK↓, 1,   ERK↑, 2,   p‑ERK↓, 1,   p‑ERK↑, 2,   FGF↑, 5,   GSK‐3β↓, 1,   p‑GSK‐3β↑, 1,   IGF-1↑, 1,   MSCs↑, 1,   mTOR↓, 4,   mTOR↑, 2,   mTOR↝, 1,   NOTCH↑, 1,   NOTCH1↑, 1,   p‑P70S6K↑, 1,   PI3K↓, 1,   PI3K↑, 1,   PTEN↑, 1,   RUNX2↑, 1,   RUNX2∅, 1,   STAT3↓, 2,   p‑STAT3↓, 1,   TumCG↑, 1,   TumCG∅, 1,   VGCC↑, 1,   Wnt↑, 3,  

Migration(tgid=13) ⓘ

APP∅, 1,   ARG1/2↑, 1,   Ca+2↓, 6,   Ca+2↑, 11,   Ca+2↝, 2,   Ca+2∅, 1,   i-Ca+2↓, 1,   Cartilage↑, 2,   CDK5↓, 1,   COL1∅, 1,   COL2A1↑, 2,   F-actin↑, 1,   FAK↑, 2,   ITGB1↑, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP2↑, 2,   MMP9↓, 3,   MMP9↑, 2,   MMPs↑, 1,   Netrins↑, 1,   OPN↑, 1,   PDGF↑, 1,   PKA↑, 1,   PKCδ↓, 1,   SMAD4↑, 1,   SMAD5↑, 1,   STAC2↑, 1,   TGF-β↑, 4,   TGF-β1↑, 1,   TIMP1↑, 2,   TIMP2↑, 1,   Treg lymp↓, 1,   TRPC1↑, 1,   TumCMig↑, 1,   β-catenin/ZEB1↑, 4,   β-Endo↑, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↑, 7,   angioG↝, 1,   EGR4↑, 1,   HIF-1↓, 1,   Hif1a↑, 2,   Hif1a↝, 1,   Hif1a∅, 2,   HIF2a↑, 1,   miR-34b-5p↓, 1,   NO↓, 4,   NO↑, 5,   NPY↑, 1,   PDGFR-BB↑, 1,   VEGF↓, 1,   VEGF↑, 11,   VEGFR2/KDR/Flk1↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   CellMemb↑, 1,   GLUT1↑, 2,   GLUT4↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1,   COX2/PTGS2↓, 2,   CXCc↓, 1,   GM-CSF↑, 1,   IFN-γ↓, 1,   p‑IKKα↓, 2,   IL1↓, 2,   IL1↑, 1,   IL10↑, 5,   IL17↓, 1,   IL1β↓, 6,   IL1β↑, 1,   IL2↑, 1,   IL4↑, 1,   IL6↓, 6,   IL6↑, 1,   IL8↓, 2,   Inflam↓, 30,   Inflam∅, 1,   IP-10/CXCL-10↑, 1,   p‑IκB↓, 1,   MCP1/CCL2↓, 1,   MCP1/CCL2↑, 2,   MIP‑1α/CCL3↓, 1,   mPGES-1↓, 1,   MyD88↓, 1,   NF-kB↓, 6,   p‑p65↓, 1,   PGE2↓, 3,   PGE2↑, 1,   PSA↓, 1,   TLR4↓, 1,   TNF-α↓, 8,   TNF-α↑, 1,  

Cellular Microenvironment(tgid=17) ⓘ

pH↑, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 2,   5HT↑, 2,   AChE↓, 1,   BDNF↑, 11,   NGF↑, 1,   PSD95↑, 1,   p‑tau↓, 2,  

Protein Aggregation(tgid=19) ⓘ

Aβ?, 1,   Aβ↓, 9,   Aβ∅, 2,   BACE/β-secretase↓, 1,   NLRP3↓, 2,   β-Amyloid↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioEnh↑, 4,   Dose↝, 33,   Dose∅, 1,   eff↓, 6,   eff↑, 21,   eff↝, 5,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

ALP↑, 2,   ALP∅, 1,   BloodF↑, 4,   BMD↑, 12,   BMPs↓, 1,   BMPs↑, 1,   GutMicro↑, 1,   IL6↓, 6,   IL6↑, 1,   LDH↓, 1,   NSE↑, 1,   PSA↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 2,   cardioP↑, 3,   chemoP↑, 1,   cognitive↑, 21,   cognitive∅, 1,   cytoP↑, 1,   hepatoP↑, 1,   memory↑, 19,   memory∅, 2,   Mood⇅, 1,   motorD↑, 10,   neuroP↑, 19,   OS↑, 2,   Pain↓, 8,   QoL↑, 5,   Strength↑, 1,   toxicity?, 1,   toxicity↓, 6,   toxicity∅, 9,   Weight∅, 1,  
Total Targets: 297

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

 

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