Magnetic Fields / Akt 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.
Akt, PKB-Protein kinase B: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Akt1 is involved in cellular survival pathways, by inhibiting apoptotic processes; Akt2 is an important signaling molecule in the insulin signaling pathway. It is required to induce glucose transport.

Inhibitors:
-Curcumin: downregulate AKT phosphorylation and signaling.
-Resveratrol
-Quercetin: inhibit the PI3K/AKT pathway.
-Epigallocatechin Gallate (EGCG)
-Luteolin and Apigenin: inhibit AKT phosphorylation


Scientific Papers found: Click to Expand⟱
2018- CAP,  MF,    Capsaicin: Effects on the Pathogenesis of Hepatocellular Carcinoma
- Review, HCC, NA
TRPV1↑, eff↑, Akt↓, mTOR↓, p‑STAT3↑, MMP2↑, ER Stress↑, Ca+2↑, ROS↑, selectivity↑, MMP↓, eff↑,
3464- MF,    Progressive Study on the Non-thermal Effects of Magnetic Field Therapy in Oncology
- Review, Var, NA
AntiTum↑, TumCG↓, TumCCA↑, Apoptosis↑, TumAuto↑, Diff↑, angioG↓, TumMeta↓, EPR↑, ChemoSen↑, ROS↑, DNAdam↑, P53↑, Akt↓, MAPK↑, Casp9↑, VEGFR2↓, P-gp↓,
496- MF,    Low-Frequency Magnetic Fields (LF-MFs) Inhibit Proliferation by Triggering Apoptosis and Altering Cell Cycle Distribution in Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, ZR-75-1 - in-vitro, BC, T47D - in-vitro, BC, MDA-MB-231
ROS↑, PI3K↓, Akt↓, GSK‐3β↑, Apoptosis↑, cl‑PARP↑, cl‑Casp3↑, BAX↑, Bcl-2↓, CycB/CCNB1↓, TumCCA↑, p‑Akt↓, TumCP↓, selectivity↑, eff↓,
3480- MF,    Cellular and Molecular Effects of Magnetic Fields
- Review, NA, NA
ROS↑, *Ca+2↑, *Inflam↓, *Akt↓, *mTOR↓, selectivity↑, *memory↑, *MMPs↑, *VEGF↑, *FGF↑, *PDGF↑, *TNF-α↑, *HGF/c-Met↑, *IL1↑,
3745- MFrot,  MF,    The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease
- Review, AD, NA
*neuroP↑, *ROS↓, *Inflam↓, *5HT↑, *cFos↑, *Aβ↓, *memory↑, *BDNF↑, *Ach↑, *AChE↓, *cognitive↑, *BDNF↑, *NGF↑, *β-catenin/ZEB1↑, *p‑Akt↓, *mTOR↓, *MMP1↓, *MMP9↓, *MMP-10↓, *TIMP1↑, *TIMP2↑,
3488- MFrot,  MF,    Rotating magnetic field improves cognitive and memory impairments in APP/PS1 mice by activating autophagy and inhibiting the PI3K/AKT/mTOR signaling pathway
- in-vivo, AD, NA
*cognitive↑, *memory↑, *neuroP↑, *Aβ↓, *PI3K↓, *Akt↓, *mTOR↓,
198- MFrot,  MF,    Biological effects of rotating magnetic field: A review from 1969 to 2021
- Review, Var, NA
AntiCan↑, breath↑, Pain↓, Appetite↑, Strength↑, BowelM↑, TumMeta↓, TumCCA↑, ETC↓, MMP↓, TumCD↑, selectivity↑, ROS↑, Casp3↑, TumCG↓, TumCCA↑, ChrMod↑, TumMeta↓, Imm↑, DCells↑, Akt↓, OS⇅, toxicity↓, QoL↑, hepatoP↑, Pain↓, Weight↑, Strength↑, Sleep↑, IL6↓, CD4+↑, CD8+↑, Ca+2↑, radioP↑, chemoP↑, *BMD↑, *AntiAge↑, *AMPK↑, *P21↓, *P53↓, *mTOR↓, *OS↑, *β-Endo↑, *5HT↓,
225- MFrot,  MF,    Extremely low frequency magnetic fields regulate differentiation of regulatory T cells: Potential role for ROS-mediated inhibition on AKT
- vitro+vivo, Lung, NA
MMP2↓, MMP9↓, FOXP3↓, ROS↑, p‑Akt↓,

Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 6,  

Mitochondria & Bioenergetics ⓘ

ETC↓, 1,   MMP↓, 2,  

Cell Death ⓘ

Akt↓, 4,   p‑Akt↓, 2,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   Casp9↑, 1,   MAPK↑, 1,   TRPV1↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

BowelM↑, 1,   ChrMod↑, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↓, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1,   GSK‐3β↑, 1,   mTOR↓, 1,   PI3K↓, 1,   p‑STAT3↑, 1,   TumCG↓, 2,  

Migration ⓘ

Ca+2↑, 2,   MMP2↓, 1,   MMP2↑, 1,   MMP9↓, 1,   TumCP↓, 1,   TumMeta↓, 3,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EPR↑, 1,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   DCells↑, 1,   FOXP3↓, 1,   IL6↓, 1,   Imm↑, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   Appetite↑, 1,   breath↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   OS⇅, 1,   Pain↓, 2,   QoL↑, 1,   radioP↑, 1,   Sleep↑, 1,   Strength↑, 2,   toxicity↓, 1,   Weight↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 64

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,  

Cell Death ⓘ

Akt↓, 2,   p‑Akt↓, 1,   HGF/c-Met↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,  

DNA Damage & Repair ⓘ

P53↓, 1,  

Cell Cycle & Senescence ⓘ

P21↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

cFos↑, 1,   FGF↑, 1,   mTOR↓, 4,   PI3K↓, 1,  

Migration ⓘ

Ca+2↑, 1,   MMP-10↓, 1,   MMP1↓, 1,   MMP9↓, 1,   MMPs↑, 1,   PDGF↑, 1,   TIMP1↑, 1,   TIMP2↑, 1,   β-catenin/ZEB1↑, 1,   β-Endo↑, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL1↑, 1,   Inflam↓, 2,   TNF-α↑, 1,  

Synaptic & Neurotransmission ⓘ

5HT↓, 1,   5HT↑, 1,   AChE↓, 1,   BDNF↑, 2,   NGF↑, 1,  

Protein Aggregation ⓘ

Aβ↓, 2,  

Clinical Biomarkers ⓘ

BMD↑, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   cognitive↑, 2,   memory↑, 3,   neuroP↑, 2,   OS↑, 1,  
Total Targets: 38

Scientific Paper Hit Count for: Akt, PKB-Protein kinase B
8 Magnetic Fields
4 Magnetic Field Rotating
1 Capsaicin
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#:4  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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