condition found tbRes List
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


TumCCA, Tumor cell cycle arrest: Click to Expand ⟱
Source:
Type:
Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases. S, G1, G2, and M are the four phases of mitosis.
Scientific Papers found: Click to Expand⟱
3477- MF,    Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis
- Review, NA, NA
*Ca+2↑, When cells are subjected to external mechanical stimulation, voltage-gated ion channels in the cell membrane open and intracellular calcium ion concentration rises
*VEGF↑, BMSCs EMF combined with VEGF promote osteogenesis and angiogenesis
*angioG↑,
Ca+2↑, 1 Hz/100 mT MC4-L2 breast cancer cells EMF lead to calcium ion overload and ROS increased, resulting in necroptosis
ROS↑,
Necroptosis↑,
TumCCA↑, 50 Hz/4.5 mT 786-O cells ELF-EMF induce G0/G1 arrest and apoptosis in cells lines
Apoptosis↑,
*ATP↑, causing the ATP or ADP increases, and the purinergic signal can upregulate the expression of P2Y1 receptors
*FAK↑, Our research team [53] found that ELE-EMF can induce calcium oscillations in bone marrow stem cells, up-regulated calcium ion activates FAK pathway, cytoskeleton enhancement, and migration ability of stem cells in vitro is enhanced.
*Wnt↑, ability of EMF to activate the Wnt10b/β-catenin signaling pathway to promote osteogenic differentiation of cells depends on the functional integrity of primary cilia in osteoblasts.
*β-catenin/ZEB1↑,
*ROS↑, we hypothesize that the electromagnetic field-mediated calcium ion oscillations, which causes a small amount of ROS production in mitochondria, regulates the chondrogenic differentiation of cells, but further studies are needed
p38↑, RF-EMF was able to suppress tumor stem cells by activating the CAMKII/p38 MAPK signaling pathway after inducing calcium ion oscillation and by inhibiting the β-catenin/HMGA2 signaling pathway
MAPK↑,
β-catenin/ZEB1↓,
CSCs↓, Interestingly, the effect of electromagnetic fields is not limited to tumor stem cells, but also inhibits the proliferation and development of tumor cells
TumCP↓,
ROS↑, breast cancer cell lines exposed to ELE-EMF for 24 h showed a significant increase in intracellular ROS expression and an increased sensitivity to further radiotherapy
RadioS↑,
Ca+2↑, after exposure to higher intensity EMF radiation, showed a significant increase in intracellular calcium ion and reactive oxygen species, which eventually led to necroptosis
eff↓, while this programmed necrosis of tumor cells was able to be antagonized by the calcium blocker verapamil or the free radical scavenger n -acetylcysteine
NO↑, EMF can regulate multiple ions in cells, and calcium ion play a key role [92, 130], calcium ion acts as a second messenger that can activate downstream molecules such as NO, ROS

508- MF,  doxoR,    Synergistic cytotoxic effects of an extremely low-frequency electromagnetic field with doxorubicin on MCF-7 cell line
- in-vitro, BC, MCF-7
ROS↑,
Apoptosis↑,
TumCCA↑, enhanced arrest of MCF-7 cells in the G0-G1 phase

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↓, growth inhibition (∼5%)
TumVol↓, 9% for PMF2
Casp3↑,
Casp7↑,
Apoptosis↑,
DNAdam↑,
TumCCA↑,
ChemoSen↑, PEMF synergistically enhances the potency of chemotherapy agents such as doxorubicin, 17 vincristine, 18 mitomycin C, 18 cisplatin, 18 and actinomycin.
EPR↑, PEMF can increase cell permeability. longer PEMF exposure may be required to increase cell membrane permeability.

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↑, attenuated by ROS scavenger NAC
PI3K↓,
Akt↓,
GSK‐3β↑,
Apoptosis↑,
cl‑PARP↑, cleaved PARP-1
cl‑Casp3↑,
BAX↑,
Bcl-2↓,
CycB↓, Cyclin B1
TumCCA↑, failure of the transition from the G2 phase to M phase
p‑Akt↓,
p‑Akt↓,

487- MF,    Extremely Low-Frequency Electromagnetic Fields Cause G1 Phase Arrest through the Activation of the ATM-Chk2-p21 Pathway
- in-vitro, NMSC, HaCaT
ATM↑,
Chk2↑,
P21↑,
TumCCA↑, cause G1 arrest and decrease colony formation

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

356- SNP,  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


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Results for Effect on Cancer/Diseased Cells:
Akt↓,1,   p‑Akt↓,2,   angioG↓,1,   Apoptosis↑,5,   ATM↑,1,   BAX↑,1,   Bcl-2↓,2,   Ca+2↑,2,   Casp3↑,1,   cl‑Casp3↑,1,   Casp7↑,1,   Catalase↑,1,   ChemoSen↑,1,   Chk2↑,1,   CSCs↓,1,   CycB↓,1,   DNAdam↑,1,   eff↓,1,   eff↑,1,   EPR↑,1,   GSK‐3β↑,1,   HSP70/HSPA5↓,1,   HSP90↓,1,   iNOS↑,1,   MAPK↑,1,   Necroptosis↑,1,   NF-kB↑,1,   NO↑,1,   other↓,1,   other↑,1,   P21↑,1,   p38↑,1,   P53↑,1,   cl‑PARP↑,1,   PI3K↓,1,   RadioS↑,1,   ROS↑,5,   SOD↑,1,   TumCCA↑,7,   TumCG↓,1,   TumCMig↓,1,   TumCP↓,2,   TumVol↓,2,   VEGFR2↓,1,   β-catenin/ZEB1↓,1,  
Total Targets: 45

Results for Effect on Normal Cells:
angioG↑,1,   ATP↑,1,   Ca+2↑,1,   FAK↑,1,   ROS↑,1,   VEGF↑,1,   Wnt↑,1,   β-catenin/ZEB1↑,1,  
Total Targets: 8

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest
7 Magnetic Fields
1 doxorubicin
1 Silver-NanoParticles
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:172  Target#:322  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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