CellMemb Cancer Research Results
CellMemb, Cellular Membrane permeability: Click to Expand ⟱
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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.
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Scientific Papers found: Click to Expand⟱
AntiCan↑, AgNPs are employed in newly emerging applications as photosensitizers/radiosensitizers, antiviral and anticancer agents.
RadioS↑,
CellMemb↑, underlying anticancer mechanisms of AgNPs include (1) disruption of cell membranes, and (2) production of reactive oxygen species and Ag+ to damage protein or DNA.
ROS↑,
DNAdam↑,
PhotoS↑, photosensitizing mechanism of AgNPs is based on nonradiative decay converting photo energy to thermal energy.
eff↑, Smaller particles have a larger surface area and, therefore, have greater toxic potential
chemoP↑, These compounds have been shown to effectively treat heart diseases and inhibit cancer cell growth while also alleviating chemotherapy side effects.
TumCG↓,
eff↑, anzroot plant can be effectively used as a reducing agent for AgNPs synthesis, and AgNPs have the potential to be used effectively in cancer therapy methods and to inhibit the growth of cancer cells.
CellMemb↑, As the AgNPs concentration increased, the permeability of the membrane increased
selectivity↑, Cancer cells exhibit higher permeability and retention, allowing for preferential interaction with SNPs due to their nanoscale size
ROS↑, AgNPs respond to intracellular signaling through ROS activation, and p53-mediated apoptosis is notably effective when using AgNPs
P53↑,
Apoptosis↑,
ROS↑,
CellMemb↑, damage
CellMemb↑, Over 30 years ago, electric fields were shown to transiently permeabilize plasma membranes and to introduce deoxyribonucleic acid (DNA) into cells by electroporation.
Ca+2↑, NsPEFs have been shown to breach intracellular granules,9 to mobilize Ca2+ from the ER and through plasma membranes,18–20 and to modulate intracellular Ca2+ levels in chromaffin cells
ER Stress↑,
ROS↑, NsPEFs induce calcium-dependent reactive oxygen species, which appear to require calcium entry through the plasma membrane pores.
MMP↓, NsPEFs also cause a rapid time- and electric field-dependent dissipation of the mitochondria membrane potential (∆Ψm).
VGCC↓, It has been shown that nsPEFs inhibit voltage-gated Na+ and Ca2+ channels,35
VGSC↓,
Dose↝, What seems clear is that when used at low repetition rates (1–2 Hz), nsPEF-induced cell death is not thermal nor immediate, but somewhat calculated and finally, default-driven.
*CellMemb↑, 300-ns pulses at 1.8 and 2.3 kV/cm caused permeabilization in HEK2913 cells. Exposure at 2.3 kV/cm caused permeabilization in all cells tested.
*VGCC↑, Voltage-gated Ca2+ channels (VGCC) are one of the major transmembrane pathways for Ca2+ to enter the cell.These channels are activated by membrane depolarization,
*Ca+2↑, ability of nsPEF to elevate cytosolic Ca2+ by nanopore opening could become a promising approach for non-chemical triggering of Ca2+-signaling in various cell types.
*MMP↓, These channels are activated by membrane depolarization,
*VGCC⇅, Aside from the immediate VGCC activation by membrane depolarization, nsPEF-treated cells experienced a long-lasting inhibition of VGCC
eff↑, Permeabilization by nsPEF is stronger in cells which express more VGCC
CellMemb↑, In this work, nsPEF treatment is used to demonstrate changes that affect viability, plasma membrane permeability ROS (Reactive Oxygen Species) in the cytosol and mitochondria, and Electron Transport Chain (ETC) in cell cultures.
ROS↑, nsPEF and rotenone synergistically enhanced ROS production in intact cells suggesting that nsPEF and rotenone act at different Complex I sites.
ETC↝, A reduced cellular oxygen consumption after nsPEFs treatment indicates an alteration of the ETC at Complex I in intact and permeabilized cells as well as in isolated hepatocyte mitochondria
OCR↓,
MMP↓, collapse the mitochondrial membrane potential and cause cell death.
ETC↓, NsPEFs attenuated electron transport (ET) (O2 consumption) in the electron transport chain (ETC) of intact and permeabilized cells
OCR↓,
CellMemb↑,
mt-ROS↑, Effects of nsPEFs on increases in mROS were synergistic with the complex I inhibitor rotenone
MMP↓, dissipating the ΔΨm
OS↑, A statistically greater overall survival fraction was noted in the high-dose H-FIRE + liposomal doxorubicin
CellMemb↑, defects facilitate an increase in cell membrane permeability
Imm↑, non-thermal cell death mechanism induced by IRE can improve upon the antigen presentation and consequently the immune response
Inflam↓, cell death is in part pro-inflammatory (necrosis and pyroptosis),
necrosis↑,
Pyro↑,
eff↑, H-FIRE utilizes bursts of biphasic pulsed electric fields to non-thermally ablate neoplastic and non-neoplastic tissue while mitigating excitation of skeletal muscle and nerves during tissue ablation.
IL2↑, IFNγ, interleukin-2 (IL-2) (p< 0.01), interleukin-6 (IL-6) (p< 0.01), and interleukin-17a (IL-17a) (p< 0.001) were significantly elevated in rats treated with H-FIRE ablation
IL6↑,
IL17↑,
IFN-γ↓,
CellMemb↑, Ultrashort nanosecond-domain pulses can exhibit unique intracellular effects because they are able to penetrate into cells and organelles.
Ca+2↑, The most important ion for cell signaling is Ca2+, and the cytoplasmic concentration of Ca2+ has been observed to transiently increase with every NPS pulse.
Imm↑, They present the promise of the dual effect of eliminating the primary tumor while triggering an adaptive immune response that could eliminate metastases as well.
TumMeta↓,
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Melanoma, |
B16-F10 |
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TumCD↑, Nano-Pulse Stimulation™ Therapy (NPS™) is a new, bioelectric modality that applies ultrashort pulses of electric energy to trigger regulated cell death in treated tissues.
eff↑, NPS permanently eliminated up to 91% of all tumor lesions with a single treatment compared to cryoablation that only eliminated up to 66%.
MusCon↓, with minimal dermal fibrosis, underlying muscle atrophy, permanent hair follicle loss or other markers of permanent skin damage.
CellMemb↑, NPS is a bioelectric energy modality that triggers the cell’s natural self-destruct pathway by initiating a transient permeabilization of the plasma and organelle membranes of targeted cells without causing thermal damage.
ER Stress↑, NPS is a bioelectric energy modality that triggers the cell’s natural self-destruct pathway by initiating a transient permeabilization of the plasma and organelle membranes of targeted cells without causing thermal damage.
other↝, The current lesion size limitation is 1 cm in diameter for a single treatment, but larger lesions can be treated with multiple applications
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in-vivo, |
PC, |
Panc02 |
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in-vivo, |
BC, |
4T1 |
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CellMemb↑, ultrashort electric pulses generate nanopores in both the plasma membrane and organelle membranes of treated tissues, increasing intracellular calcium, initiating DNA fragmentation and protein hydrolysis
Ca+2↑,
DNAdam↑,
eff↝, If the tumors can be imaged with high resolution, effective treatment will rely upon accurate positioning of the applicator electrodes to encompass the entire tumor and deliver energy uniformly
Imm↑, generate an immune response such as antibodies and cytotoxic CD8+ T cells specific for the detected antigens.
other↝, Figure 1, equivalent electrical circuit
ROS↑, Another aspect to consider is the fact that PEF application has been shown to result in reactive oxygen species (ROS) production not only in cells71,72 but also in the medium surrounding the cells
Temp∅, Provided the number of pulses and the PRF are not too high, allowing for interpulse heat dissipation, in most cases, thermal effects can even be neglected.
CellMemb↑, he main primary effect of nsPEFs is the permeabilization of both the cell membrane82 and organelle membranes, followed by calcium entry,83 loss of resting membrane potential,62,84 increased cellular K+ efflux,84 activation of VGCC ion channels
Ca+2↑, In addition to apoptosis, nsPEFs are known to trigger calcium mobilization.
Apoptosis↑, The apoptosis is characterized by several morphological changes in the cell, due to energy-dependent biochemical mechanisms, leading to cell death
TumCD↑,
MMP↓, , while the dissipation of ψ (mitochondria membrane potential) occurs at a higher level (around 40 kV/cm)
necrosis↑, A severe dysregulation of Ca2+ stimulates a cell death by necrosis, while a milder dysregulation provokes a cell death by apoptosis.103
TumVol↓, As a result, tumor shrinkage of 90% could be observed within 2 weeks, and the repetition of a second treatment at that time could result in complete regressions.
Remission↑,
Ca+2↑, Ca2+ overload→ATP depletion→mitochondrial dysfunction
ATP↓,
mtDam↑,
ROS↑, ROS generation from mitochondrial leakage disrupts cell homeostasis.
CellMemb↑, EP: membrane permeabilization→drug uptake↑;
Ca+2↑, leading to an incremental increase in cytoplasmic Ca2+ concentration,
Apoptosis↑, from apoptosis up to cell differentiation and proliferation.
Diff↑,
TumCP↓,
Wound Healing↑, sterilization in the food industry, seed germination, anti-parasitic effects, wound healing, increased immune response
CellMemb↑, available evidence suggest that the increase in cytoplasmic Ca2+ concentration produced by the application of nsPEF could be due to the formation of membrane nanopores.
VGCC↑, most probable cause should be the increase of intracellular Ca2+ concentration via VGCC activation [185].
VGSC↑, findings relating VGNC activation by nsPEF are exciting and deserve more attention.
DNAdam↑, Stacey et al. in 2002 demonstrated that exposing cancer cells to nsPEF with 60 kV/cm could induce DNA damage [243]
selectivity↑, More importantly for nsPEF as cancer treatment, tumor cells are more sensitive to nsPEF than normal cells [246].
AntiCan↑, Nanosecond pulsed electric fields (nsPEF) have been shown to exert anticancer effects
Dose↝, 200 ns, 100 pulses, 8 kV/cm, 10 kHz PEF treatment.
CellMemb↑, electropermeabilization in EPP85-181RNOV cells
ChemoSen↑, leading to a transient increase in vulnerability of the cells towards paclitaxel.
MMP↓, Noteworthy, membrane signal after PEF treatment was highly reduced in comparison to the control sample.
Apoptosis↑,
CellMemb↑, damage
CellMemb↑, Induce Tumor Membrane Disruption
TumCP↓, but not that of normal lymphatic cells. ****
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in-vitro, |
AML, |
THP1 |
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in-vitro, |
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PC12 |
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in-vivo, |
Cerv, |
HeLa |
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H2O2↑, These results suggest that ELF MF stimulation facilitates H2O2-dependent cell death in cancer cells as its effect was enhanced nearly two-fold
TumCD↑, 1 μM MTX
CellMemb↑,
eff↑, ELF-MF enhance the effects of methotrexate on THP-1 and PC12 cells
*Dose↝, The ED50 is 15 mT, with a 95% confidence interval of 6.50-34.9 mT.
*CellMemb↑, These results indicate that a static magnetic field of 10 mT or greater can increase passive transport in phospholipid membrane bilayers maintained at or near their membrane phase-transition temperature.
*other↝, Lipid clustering which occurs at prephase-transition temperatures may predispose phospholipid domains to diamagnetic orientation in a magnetic field and thereby facilitate drug release.
Dose↑, pulsed magnetic field (MF) (3.5 T, 1 Hz, 8 square-wave/160 µs)
CellMemb↑, Uptake of BLM molecules by tumoral cells in the BLM plus 3.5 T MF group versus the BLM control group was 7- folds higher
eff↝, Significant cell permeabilization to BLM requires greater MF strength or exposure time.
other↝, pulsed low electric fields (2.5-20 V/cm) can increase cell membrane permeability by up to 10-fold. induced electric field intensity caused by an alternating magnetic field at 3.5 T is 7.5 V/cm at a 1cm distance from the probes
TumCG↓, figure 1
Dose↝, After 60 min of exposure to 7 Hz sinusoidal (50 mu T peak) and parallel static (50 mu T) magnetic fields the enzyme activity, as a function of increased diffusion rate of p-NPA, rose from 17 +/- 3% to 80 +/- 9% (P < .0005, n = 15) in the 5:3:2 liposo
CellMemb↑, Such studies suggest a plausible link between the action of extremely low frequency magnetic field on charged lipids and a change of membrane permeability.
CellMemb↑, damage the cell membrane
lysoMP↑, through heat and/or mechanical damage
ERK↑,
Apoptosis↑,
lysoMP↓, damage
CellMemb↑, Physical destruction of cell membrane
CellMemb↑, higher water absorption
GlucoseCon↓, The bacteria exposed to the RMF used 9% less glucose as compared with the microorganisms from the control culture
CellMemb↑, more negatively charged outer membrane.
Improves adsorption thru cell membrane.
Showing Research Papers: 1 to 25 of 25
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 25
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
H2O2↑, 1, ROS↑, 7, mt-ROS↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↓, 1, ETC↓, 1, ETC↝, 1, MMP↓, 5, mtDam↑, 1, OCR↓, 2,
Core Metabolism/Glycolysis ⓘ
GlucoseCon↓, 1,
Cell Death ⓘ
Apoptosis↑, 5, lysoMP↓, 1, lysoMP↑, 1, necrosis↑, 2, Pyro↑, 1, TumCD↑, 3,
Transcription & Epigenetics ⓘ
other↝, 3, PhotoS↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 2,
DNA Damage & Repair ⓘ
DNAdam↑, 3, P53↑, 1,
Proliferation, Differentiation & Cell State ⓘ
Diff↑, 1, ERK↑, 1, TumCG↓, 2, VGCC↓, 1, VGCC↑, 1, VGSC↓, 1, VGSC↑, 1,
Migration ⓘ
Ca+2↑, 6, TumCP↓, 2, TumMeta↓, 1,
Barriers & Transport ⓘ
CellMemb↑, 23,
Immune & Inflammatory Signaling ⓘ
IFN-γ↓, 1, IL17↑, 1, IL2↑, 1, IL6↑, 1, Imm↑, 3, Inflam↓, 1,
Cellular Microenvironment ⓘ
Temp∅, 1,
Drug Metabolism & Resistance ⓘ
ChemoSen↑, 1, Dose↑, 1, Dose↝, 3, eff↑, 6, eff↝, 2, RadioS↑, 1, selectivity↑, 2,
Clinical Biomarkers ⓘ
IL6↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, chemoP↑, 1, MusCon↓, 1, OS↑, 1, Remission↑, 1, TumVol↓, 1, Wound Healing↑, 1,
Total Targets: 54
Pathway results for Effect on Normal Cells:
Mitochondria & Bioenergetics ⓘ
MMP↓, 1,
Transcription & Epigenetics ⓘ
other↝, 1,
Proliferation, Differentiation & Cell State ⓘ
VGCC↑, 1, VGCC⇅, 1,
Migration ⓘ
Ca+2↑, 1,
Barriers & Transport ⓘ
CellMemb↑, 2,
Drug Metabolism & Resistance ⓘ
Dose↝, 1,
Total Targets: 7
Scientific Paper Hit Count for: CellMemb, Cellular Membrane permeability
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
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