condition found
Features: |
Rotary Magnetic field can be generated by a spinning magnet or magnets. Or it can be implemented with 2 or more coils, power with a phase shift between them (90 deg for 2 coil implementation) (60deg for 3 coil implementation) Targets affected are mostly the same as for Magnet fields Main differences - may enhance the EPR effect allowing targeting of drugs to cancer cells - acts as wireless stirrer, especially on magnetic particles(inducing eddy currents in water media) - research for use in nano surgery, and mechanical destruction of cancer cells - continue to highlight ability to raise ROS in cancer cell and lower ROS in normal cells - RMF may be responsible for Ca2+ distribution to pass across the plasma membrane(differental affected for cancer and normal cells) Pathways: - induce ROS production in cancer cells, while decreasing ROS in normal cells. Ca2+ is critical and the Ca2+ balance is increased in cancer cells while decreased in normal cells (example for wound healing) - ROS↑ related: MMP↓(ΔΨm), 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↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, - inhibit Growth/Metastases : TumMeta↓, TumCG↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, RhoA↓, NF-κB↓, TGF-β↓, ERK↓ - cause Cell cycle arrest : TumCCA↑, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, - Others: PI3K↓, AKT↓, Wnt↓, AMPK, ERK↓, JNK, - Synergies: < Others(review target notes), Neuroprotective, Cognitive, - Selectivity: Cancer Cells vs Normal Cells |
Source: HalifaxProj(inhibit) CGL-CS TCGA |
Type: |
Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses. Anti-inflammatory cytokine. In normal tissues, TGF-β plays an essential role in cell cycle regulation, immune function, and tissue remodeling. - In early carcinogenesis, TGF-β typically acts as a tumor suppressor by inhibiting cell proliferation and inducing apoptosis. In advanced cancers, cells frequently become resistant to the growth-inhibitory effects of TGF-β. - TGF-β then switches roles and promotes tumor progression by stimulating epithelial-to-mesenchymal transition (EMT), cell invasion, metastasis, and immune evasion. Non-canonical (Smad-independent) pathways, such as MAPK, PI3K/Akt, and Rho signaling, also contribute to TGF-β-mediated responses. Elevated levels of TGF-β have been detected in many advanced-stage cancers, including breast, lung, colorectal, pancreatic, and prostate cancers. - The switch from a tumor-suppressive to a tumor-promoting role is often associated with increased TGF-β production and activation in the tumor microenvironment. High TGF-β expression or signaling activity is frequently correlated with aggressive disease features, resistance to therapy, increased metastasis, and poorer overall survival in many cancer types. |
3497- | MFrot,  |   | The Effect of a Rotating Magnetic Field on the Regenerative Potential of Platelets |
- | Human, | Nor, | NA |
201- | MFrot,  |   | Gradient Rotating Magnetic Fields Impairing F-Actin-Related Gene CCDC150 to Inhibit Triple-Negative Breast Cancer Metastasis by Inactivating TGF-β1/SMAD3 Signaling Pathway |
- | in-vitro, | BC, | MDA-MB-231 | - | in-vitro, | BC, | BT549 | - | in-vitro, | BC, | MDA-MB-468 |
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:192 Target#:304 State#:% Dir#:%
wNotes=on sortOrder:rid,rpid