Magnetic Fields / Casp7 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.
Casp7, Caspase-7: Click to Expand ⟱
Source:
Type:
Members of the caspase family of proteases play essential roles in the initiation and execution of apoptosis. These caspases are divided into two groups: the initiator caspases (caspase-2, −8, −9 and −10), which are the first to be activated in response to a signal, and the executioner caspases (caspase-3, −6, and −7) that carry out the demolition phase of apoptosis. Downregulation of caspase-3 is an effective apoptosis-evading mechanism frequently observed in cancer cells in association with acquired chemoresistance to apoptosis-inducing anticancer drugs. Indeed, re-expression of caspase-3 often restores sensitivity to apoptosis.
Caspase-7:
Role: Executioner caspase similar to caspase-3.
Cancers: Expression levels can vary; often studied in breast and prostate cancers.
Prognosis: Its prognostic value is less clear and may depend on the cancer type.
Scientific Papers found: Click to Expand⟱
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∅, Apoptosis↑, Casp↑, tumCV↓, Casp3↑, Casp7↑, Ca+2↑, Cyt‑c↑,
497- MF,    In Vitro and in Vivo Study of the Effect of Osteogenic Pulsed Electromagnetic Fields on Breast and Lung Cancer Cells
- vitro+vivo, NA, MCF-7 - vitro+vivo, NA, A549
TumCG↓, TumVol↓, Casp3↑, Casp7↑, Apoptosis↑, DNAdam↑, TumCCA↑, ChemoSen↑, EPR↑,
506- MF,  doxoR,    Pulsed Electromagnetic Field Stimulation Promotes Anti-cell Proliferative Activity in Doxorubicin-treated Mouse Osteosarcoma Cells
- in-vitro, OS, LM8
TumCP↓, p‑CHK1↓, Ca+2↑, Casp3↓, Casp7↓, p‑BAD↓, ChemoSen↑,
4353- MF,  Chemo,    Pulsed Electromagnetic Field Enhances Doxorubicin-induced Reduction in the Viability of MCF-7 Breast Cancer Cells
- in-vitro, BC, MCF-7
TumCCA↑, Apoptosis↑, eff↑, TumCCA↑, Casp↝, p‑CDK2↓, cycE/CCNE↓, Fas↑, BAX↑, survivin↓, Mcl-1↓, cl‑PARP↑, cl‑Casp7↑, cl‑Casp8↑, cl‑Casp9↑,
3486- MF,    Pulsed electromagnetic field potentiates etoposide-induced MCF-7 cell death
- in-vitro, NA, NA
ChemoSen↑, tumCV↓, cl‑PARP↑, Casp7↑, Casp9↑, survivin↓, BAX↑, DNAdam↑, ROS↑, eff↓,
184- MFrot,  MF,    Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells
- in-vitro, GBM, GBM
ROS↑, mitResp↓, mtDam↑, Dose↝, MMP?, OCR↓, mt-H2O2↑, eff↓, SDH↓, Thiols↓, GSH↓, TumCD↑, Casp3↑, Casp7↑, MPT↑, Cyt‑c↑, selectivity↑, GSH/GSSG↓, ETC↓,

Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   GSH/GSSG↓, 1,   mt-H2O2↑, 1,   ROS↑, 2,   Thiols↓, 1,  

Mitochondria & Bioenergetics ⓘ

ETC↓, 1,   mitResp↓, 1,   MMP?, 1,   MPT↑, 1,   mtDam↑, 1,   OCR↓, 1,   SDH↓, 1,  

Cell Death ⓘ

Apoptosis↑, 3,   p‑BAD↓, 1,   BAX↑, 2,   Casp↑, 1,   Casp↝, 1,   Casp3↓, 1,   Casp3↑, 3,   Casp7↓, 1,   Casp7↑, 4,   cl‑Casp7↑, 1,   cl‑Casp8↑, 1,   Casp9↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 2,   Fas↑, 1,   Mcl-1↓, 1,   survivin↓, 2,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

DNA Damage & Repair ⓘ

p‑CHK1↓, 1,   DNAdam↑, 2,   cl‑PARP↑, 2,  

Cell Cycle & Senescence ⓘ

p‑CDK2↓, 1,   cycE/CCNE↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 2,   TumCP↓, 1,  

Angiogenesis & Vasculature ⓘ

EPR↑, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 3,   Dose↝, 1,   Dose∅, 1,   eff↓, 2,   eff↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

TumVol↓, 1,  
Total Targets: 48

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Casp7, Caspase-7
6 Magnetic Fields
1 Iron
1 doxorubicin
1 Chemotherapy
1 Magnetic Field Rotating
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#:43  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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