Magnetic Fields / CellMemb 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↓, 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.
CellMemb, Cellular Membrane permeability: Click to Expand ⟱
Source:
Type:
The cell membrane, also called the plasma membrane, is a thin layer that surrounds the cell. It is a selectively permeable cell organelle, allowing certain substances inside the cell while preventing others to pass.
Scientific Papers found: Click to Expand⟱
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↑, TumCD↑, CellMemb↑, eff↑,
495- MF,    How a High-Gradient Magnetic Field Could Affect Cell Life
- in-vitro, NA, HeLa
Apoptosis↑, CellMemb↑,
515- MF,    Pulsed Low-Frequency Magnetic Fields Induce Tumor Membrane Disruption and Altered Cell Viability
- in-vitro, Lung, A549
CellMemb↑, TumCP↓,
5533- MF,    Magnetic field-induced drug permeability in liposome vesicles
- in-vitro, Nor, NA
*Dose↝, *CellMemb↑, *other↝,
5532- MF,    Magnetoporation: New Method for Permeabilization of Cancerous Cells to Hydrophilic Drugs
- in-vivo, BC, NA
Dose↑, CellMemb↑, eff↝, other↝, TumCG↓,
5531- MF,    Effect of low frequency, low amplitude magnetic fields on the permeability of cationic liposomes entrapping carbonic anhydrase: I. Evidence for charged lipid involvement
- in-vitro, NA, NA
Dose↝, CellMemb↑,
189- MFrot,  MF,    Cancer treatment by magneto-mechanical effect of particles, a review
- Review, Var, NA
CellMemb↑, lysoMP↑, ERK↑, Apoptosis↑,
213- MFrot,  MF,    Rotating Magnetic Field-Assisted Reactor Enhances Mechanisms of Phage Adsorption on Bacterial Cell Surface
- in-vitro, NA, NA
CellMemb↑,
216- MFrot,  MF,    Elongated Nanoparticle Aggregates in Cancer Cells for Mechanical Destruction with Low Frequency Rotating Magnetic Field
- in-vitro, GBM, U87MG
lysoMP↓, CellMemb↑,
214- MFrot,  MF,    Modification of bacterial cellulose through exposure to the rotating magnetic field
- in-vitro, Nor, NA
CellMemb↑, GlucoseCon↓,

Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

H2O2↑, 1,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon↓, 1,  

Cell Death ⓘ

Apoptosis↑, 2,   lysoMP↓, 1,   lysoMP↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↑, 1,   TumCG↓, 1,  

Migration ⓘ

TumCP↓, 1,  

Barriers & Transport ⓘ

CellMemb↑, 9,  

Drug Metabolism & Resistance ⓘ

Dose↑, 1,   Dose↝, 1,   eff↑, 1,   eff↝, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Transcription & Epigenetics ⓘ

other↝, 1,  

Barriers & Transport ⓘ

CellMemb↑, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,  
Total Targets: 3

Scientific Paper Hit Count for: CellMemb, Cellular Membrane permeability
10 Magnetic Fields
4 Magnetic Field Rotating
1 methotrexate
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#:532  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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