MPT Cancer Research Results

MPT, mitochondrial permeability transition: Click to Expand ⟱

Source:

Type:

MPT refers to an alteration in the permeability of the inner mitochondrial membrane (IMM), Mitochondrial permeability transition (MPT) refers to a process involving the opening of the mitochondrial permeability transition pore (mPTP), which can lead to the loss of mitochondrial membrane potential, disruption of ATP synthesis, and release of pro-apoptotic factors into the cytosol. This process is critical in various physiological and pathological contexts, including cancer.

Mitochondrial permeability transition plays a significant role in cancer biology, with its dysregulation often associated with poor prognosis and protumorigenic effects. The specific roles of MPT can vary by cancer type and context.

Scientific Papers found: Click to Expand⟱

5266-

3BP,

3-bromopyruvate-based agent KAT-101

Review,

Var,

eff↑, Upon oral administration of 3-BP-based agent KAT-101, the 3-BP derivative, being structurally similar to lactic acid, specifically binds to and enters cancer cells through monocarboxylic acid transporters (MCTs)
Glycolysis↓, KAT-101 interferes with both glycolysis and mitochondrial oxidative phosphorylation (OxPhos), thereby depleting adenosine triphosphate (ATP) levels and thus limits energy supply needed by cancer cells to proliferate.
OXPHOS↓,
ATP↓,
TumCP↓,
Apoptosis↑, This induces cancer cell apoptosis and prevents cancer cell proliferation.
HK2↓, In addition, KAT-101 is able to release mitochondrial-bound hexokinase (HK) II (HK2)
MPT↑, increases the formation of mitochondrial permeability transition pores (MPTPs), which induces apoptosis.
LDH↓, KAT-101 also inhibits a variety of enzymes, including lactate dehydrogenase (LDH), pyruvate dehydrogenase (PDH) and pyruvate dehydrogenase kinase (PDHK).
PDH↓,

5978-

AgNPs,

Biological synthesis of silver nanoparticles and their medical applications

Review,

Var,

Wound Healing↑, The notable antimicrobial properties of silver render it indispensable for wound healing, infection control, cancer therapy and tissue regeneration applications.
AntiCan↑,
other↑, Additionally, AgNPs hold great promise as versatile drug carriers for targeted therapies and as contrast agents for advanced medical imaging techniques
MPT↑, these nanoparticles exert their effects by disrupting cell membrane permeability, interfering with cellular respiration processes and instigating the production of free radicals.
ROS↑,
other↑, Additionally, it has been proposed that AgNPs may release silver ions, which can bind to thiol groups found in essential enzymes, rendering them inactive
DNAdam↑, DNA typically contains sulfur, and nanoparticles may interact with these bases, potentially causing damage to the DNA molecule, and thereby contributing to cell demise

1253-

aLinA,

The Antitumor Effects of α-Linolenic Acid

Review,

NA,

PPARγ↑,
COX2↓,
E6↓,
E7↓,
P53↑,
p‑ERK↓,
p38↓,
lipid-P↑,
ROS⇅, ALA could inhibit cancer by stimulating ROS production to induce apoptosis (other places implies reduced) appropriate dose of ALA can also reduce OS by regulating SOD, CAT, GPx, GSH, and NADPH oxidase
MPT↑, directly activate mitochondrial permeability transition
MMP↓,
Cyt‑c↑, cytochrome c (cyt c) release
Casp↑,
iNOS↓,
NO↓,
Casp3↑,
Bcl-2↓,
Hif1a↓,
FASN↓,
CRP↓,
IL6↓,
IL1β↓,
IFN-γ↓,
TNF-α↓,
Twist↓,
VEGF↓,
MMP2↓,
MMP9↓,

5835-

CAP,

Capsaicin and dihydrocapsaicin induce apoptosis in human glioma cells via ROS and Ca2+-mediated mitochondrial pathway

in-vitro,

GBM,

U251

tumCV↓, Treatment of U251 glioma cells with Cap and DHC resulted in a dose- and time-dependent inhibition of cell viability and induction of apoptosis,
Apoptosis↑,
selectivity↑, whereas few effects were observed on the viability of L929 normal murine fibroblast cells.
ROS↑, The apoptosis-inducing effects of Cap and DHC in U251 cells were associated with the generation of reactive oxygen species, increased Ca2+ concentrations, mitochondrial depolarization, release of cytochrome c into the cytosol and activation of caspas
Ca+2↑, Cap and DHC treatment increases ROS generation and [Ca2+]i in U251 cells
MMP↓,
Cyt‑c↑,
Casp↑,
eff↑, DHC, an analog of Cap, inhibits the proliferation of HCT116, MCF-7 and WI38 cells more potently than Cap,
MPT↑, High levels of Ca2+ can open mitochondrial permeability transition pores, depolarize mitochondrial membrane potential, activate caspase-9 and caspase-3, initiate the mitochondrial apoptosis pathway, to induce cell apoptosis
ETC↓, Cap boosts the generation of ROS in human pancreatic cancer cells by inhibiting mitochondrial complex I and III and destroying mitochondrial functions
Casp3↑, elease of cyto c to the cytosol to activate caspase-9 and −3
Casp9↑,

5826-

CAP,

Capsaicin induces mitochondrial dysfunction and apoptosis in anaplastic thyroid carcinoma cells via TRPV1-mediated mitochondrial calcium overload

in-vitro,

Thyroid,

TRPV1↑, we reported that capsaicin (CAP), a transient receptor potential vanilloid type1 (TRPV1) agonist, inhibited the viability of anaplastic thyroid cancer cells.
tumCV↓,
Ca+2↑, Capsaicin treatment triggered Ca2+ influx by TRPV1 activation, resulting in disequilibrium of intracellular calcium homeostasis.
mtDam↑, In addition, the disruption of mitochondrial calcium homeostasis caused by capsaicin led to mitochondrial dysfunction in ATC cells
ROS↑, as evidenced by the production of mitochondrial reactive oxygen species (ROS), depolarization of mitochondrial membrane potential (ΔΨm), and opening of mitochondrial permeability transition pore (mPTP)
MMP↓,
MPT↑,
Cyt‑c↑, the resulting release of cyt c into the cytosol triggered apoptosome assembly and subsequent caspase activation and apoptosis.
Casp↑,
Apoptosis↑,

5858-

CAP,

Capsaicin as a Microbiome Modulator: Metabolic Interactions and Implications for Host Health

Review,

Nor,

Review,

AD,

*BBB↓, crosses the blood–brain barrier, alters neurotransmitter levels, and accumulates in brain regions involved in cognition.
*GutMicro↑, capsaicin appears to undergo microbial transformation and influences gut microbial composition, favoring short-chain fatty acid producers and suppressing pro-inflammatory taxa. often favoring the growth of beneficial taxa such as Ruminococcaceae, Lac
Obesity↓, These changes contribute to anti-obesity, anti-inflammatory, and potentially anticancer effects
*Inflam↓,
*AntiCan↑,
*TRPV1↑, Capsaicin is a potent agonist perceived by TRPV1, a transmembrane cation channel that functions with Ca2+.
*Ca+2↑, causes an increase in Ca2+ flux,
*antiOx↑, Capsaicin is a bioactive compound of chili peppers responsible for their spicy flavor, which also shows antioxidant, anti-obesity, analgesic, anti-inflammatory, anticarcinogenic, and cardioprotective effects
*cardioP↑,
*BioAv↓, capsaicin exhibits low systemic bioavailability due to its rapid metabolism in the liver and other tissues, resulting in a short plasma half-life of approximately 25 min in humans
*Half-Life↓,
*BioAv↝, Capsaicin’s bioavailability is determined by multiple interrelated factors, including its physicochemical properties, metabolic transformations, route of administration, and the biological context of the host, including gut microbiota composition.
*BioAv↑, For instance, polymeric micelles, liposomes, and hydroxypropyl-β-cyclodextrin complexes have demonstrated the capacity to enhance capsaicin’s oral bioavailability, prolong its plasma half-life, and improve therapeutic consistency
*neuroP↑, capsaicin exposure alters glutamate, GABA, and serotonin levels in distinct brain regions, with potential implications for neuroprotection, mood regulation, and energy metabolism.
Apoptosis↑, apoptosis is the main mechanism by which capsaicin induces cell death in cancer cells.
p38↑, capsaicin triggers a calcium flux within the cell via TRPV1, activating the p38 pathway.
ROS↑, As a result, reactive oxygen species (ROS) are produced, along with depolarization of the mitochondrial membrane potential and opening of the mitochondrial permeability transition pore.
MMP↓,
MPT↑,
Cyt‑c↑, Consequently, cytochrome c is released, the apoptosome is assembled, and caspases are activated, ultimately leading to cell death
Casp↑,
TRIB3↑, capsaicin enhances TRIB3 gene expression, which allowed an increase in the antiproliferative and proapoptotic effects of TRIB3 in cancer cells
NADH↓, Capsaicin has also been seen to downregulate and inhibit tumor-associated NADH oxidase (tNOX) and Sirtuin1 (SIRT1) in multiple cancer cell lines such as bladder cancer, which led to reduced cell growth and migration
SIRT1↓,
TumCG↓,
TumCMig↓,
TOP1↓, pointing out that capsaicin had an inhibitory effect on topoisomerases I and II, causing a reduction in metabolic activity and proliferation of a human colon cancer cell line
TOP2↓,
β-catenin/ZEB1↓, with capsaicin, the β-catenin transcription gets downregulated
*ROS↓, Capsaicin has also been proven to alleviate redox imbalance or oxidative stress, thanks to its antioxidative activity.
*Aβ↓, Alsheimer’s disease, attenuating neurodegeneration in mice by reducing amyloid-beta levels via the promotion of non-amyloidogenic processing of amyloid precursor protein

5903-

CAR,

TV,

Combined Cytotoxic Effects of Carvacrol-Based Essential Oil Formulations

in-vitro,

BC,

MDA-MB-231

BioAv↑, Combined effects of carvacrol with α-pinene, eugenol, and β-terpineol likely contributed to enhanced bioactivity.
MPT↑, Compounds such as thymol, α-pinene, eugenol, β-terpineol, and camphene have been shown to enhance membrane permeability, modulate redox signaling, potentiate ROS-mediated cell death, and amplify caspase activation
ROS↑,
Casp↑,
eff↑, including cinnamon oil (cinnamaldehyde) and peppermint oil (menthol/menthone), which may contribute to combined effects with carvacrol to modulate cellular processes
PI3K↓, In MCF-7 cells, carvacrol has been reported to inhibit the PI3K/AKT pathway, halting the cell cycle and inducing apoptosis.
Akt↓,
TumCCA↑,
Apoptosis↑,
Cyt‑c↑, decrease in membrane potential, cytochrome-c release, caspase activation, and PARP cleavage in a concentration-dependent manner
cl‑PARP↑,
MPT↑, Thymol and α-pinene can increase cell membrane permeability, thereby enhancing cytotoxic effects

5954-

CEL,

The molecular mechanisms of celecoxib in tumor development

Review,

Var,

TumCP↓, Celecoxib mainly regulates the proliferation, migration, and invasion of tumor cells by inhibiting the cyclooxygenases-2/prostaglandin E2 signal axis
TumCMig↓,
TumCI↓,
COX2↓,
p‑NF-kB↓, thereby inhibiting the phosphorylation of nuclear factor-κ-gene binding, Akt, signal transducer and activator of transcription and the expression of matrix metalloproteinase 2 and matrix metalloproteinase 9.
Akt↓,
MMP2↓,
MMP9↓,
Apoptosis↑, celecoxib could promote the apoptosis of tumor cells by enhancing mitochondrial oxidation, activating mitochondrial apoptosis process, promoting endoplasmic reticulum stress process, and autophagy.
mitResp↑,
ER Stress↑,
TumAuto↑,
ChemoSen↑, Celecoxib can also reduce the occurrence of drug resistance by increasing the sensitivity of cancer cells to chemotherapy drugs.
Inflam↓, NSAIDs achieve anti-inflammatory effects by inhibiting the activity of the inflammatory factor COX-2 and the synthesis of PGE2.
PGE2↓,
chemoPv↑, Numerous studies have confirmed that NSAIDs also have chemopreventive effects on tumors.
toxicity↓, Compared with other NSAIDs, celecoxib shows lower toxicity side effects (such as the most common gastrointestinal bleeding and gastric ulcer).[
Risk↓, Early studies have shown that celecoxib can effectively reduce the incidence of colorectal cancer, especially inhibiting the development of familial adenomatous polyposis to colorectal cancer.
PI3K↓, celecoxib can promote cancer cell apoptosis by inhibiting the signal pathway of 3-phosphoinositide-dependent kinase-1 and downstream protein kinase B (Akt) in human colon cancer cells.
RadioS↑, celecoxib enhances the sensitivity of cancer cells to radiation therapy
TumCMig↓, inhibits cancer cell migration and invasion by inhibiting the activity of C-Jun amino-terminal kinase and downregulating the expression of specific protein 1.
TumCI↓,
cJun↓,
Sp1/3/4↓,
ROS↑, Celecoxib targets mitochondria and promotes the release of ROS by significantly increased oxidative stress.
MMP↓, lead to the decrease of cell consumption and mitochondrial transmembrane potential (△ ψ m), increasing mitochondrial membrane permeability to promote the release of ROS
MPT↑,
Ca+2↑, promote Ca2+ influx, produce a higher pro-oxidation state, increase the accumulation of ROS in cancer cell mitochondria,
Glycolysis↓, inhibits the glycolysis process, ATP synthesis is significantly reduced, leading to cancer cell death.[
ATP↓,
CSCs↓, In addition to cancer cells, celecoxib can also inhibit CSCs.
Wnt/(β-catenin)↓, celecoxib can inhibit the transduction of Wnt/β-catenin signaling pathway
EMT↓, celecoxib can inhibit the process of EMT
toxicity↝, ong-term use increases the risk of hypertension among participants who already have cardiovascular risk factors.[

5994-

Chit,

Anticancer Activity of Chitosan, Chitosan Derivatives, and Their Mechanism of Action

Review,

Var,

angioG↓, Both chitosan and its various derivatives have been reported to selectively permeate through the cancer cell membranes and show anticancer activity through the cellular enzymatic, antiangiogenic, immunoenhancing, antioxidant defense mechanism, and ap
*Imm↑,
*antiOx↑,
selectivity↑, They get sequestered from noncancer cells and provide their enhanced bioavailability in cancer cells in a sustained release manner.
other↝, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
toxicity↓, The degree of deacetylation (DDA) of chitin ranges from 60 to 100 % and molecular weight of commercially obtained chitosan ranges from 3800 to 20,000 Daltons.
BioAv↑,
eff↝, exert anticancer activity with minimal toxicity on noncancer cells [13] and such activity against different cancer cell lines significantly depends upon molecular weight and DDA [
Half-Life↑, Sustained Release Mechanism
MPT↑, Chitosan MDA-MB-231 Permeation enhancement, lowering of MMP9 activity
MMP9↓,
lipid-P↑, induction of lipid peroxidation, enhanced permeation and retention (EPR) effect
EPR↑,
NK cell↑, Immunoenhancement through increase in activity of NK cells, T cells, killer lymphocytes and cytokins.
Casp3↑, Cellular apoptosis, activation of caspase-3 and caspase-8,
Casp8↑,
TumCCA↑, Cytokine signaling cell cycle arrest, ROS activation
ROS↑,
DDS↑, CMCS has been prepared as a carrier of anticancer drug such as 5- fluorouracil, curcumin, and doxorubicin
VEGF↓, decrease in VEGF level and increase in TIMP1 level after 14-day treatment of mouse serum with CMCS in vivo.
TIMP1↑,
ChemoSen↑, The paclitaxel loaded modified glycol chitosan nanoparticles in the size of 400 nm has been found to show sustained release of paclitaxel to bring about the inhibition of MCF-7 tumor growth due to EPR effect in vitro
eff↑, Chitosan-curcumin nanoformulation has been found to show anticancer activity following the apoptotic pathways associated with DNA damage, cell-cycle blockage, and elevation of ROS levels in vivo

141-

CUR,

Effect of curcumin on Bcl-2 and Bax expression in nude mice prostate cancer

in-vivo,

Pca,

PC3

 100 mg/kg, 50 mg/kg, and 25 mg/kg curcumin)

 nude mice

BAX↑, Curcumin could inhibit PC-3 growth, decrease tumor volume, reduce tumor weight, and induce cell apoptosis under the skin of nude mice by up-regulating Bax and down-regulating Bcl-2.
Bcl-2↓,
TumCG↓,
TumVol↓,
TumW↓,
Apoptosis↑,
AR↓, Curcumin can down-regulate androgen receptor transcription and expression.
Ca+2↑, Curcumin may control Bax and Bcl-2 expression to induce Ca2+ overload in the mitochondria, resulting mitochondrial permeability transition channels open,
MPT↑,

161-

CUR,

MeSA,

Enhanced apoptotic effects by the combination of curcumin and methylseleninic acid: potential role of Mcl-1 and FAK

in-vitro,

BC,

MDA-MB-231

in-vitro,

Pca,

DU145

Mcl-1↑, CUR alone
Mcl-1↓, CUR+MeSA
MPT↑,
AIF↑, An Enhanced AIF Nuclear Translocation Was Detected in the Combination-Treated MDA-MB-231 Cells
chemoPv↑, Curcumin and methylseleninic acid (MSeA) are well-documented dietary chemopreventive agents.
Apoptosis↑, Combining MSeA With Curcumin Resulted in a Significantly Enhanced Apoptotic Effect in MDA-MB-231 and DU145 Cells
ROS↑, a significantly increased ROS generation was detected in curcumin-treated cells, whereas no change was observed in MSeA-treated cells at both 3 and 6 h posttreatment.
FAK↓, Curcumin-induced FAK inhibition
STAT3↓, Previous studies showed that curcumin was capable of inhibiting activity of STAT3 and NF kB [37]. Indeed, we confirmed these effects in MDA-MB-231 cells
NF-kB↓,

4640-

HT,

The anti-cancer potential of hydroxytyrosol

Review,

Var,

selectivity↑, Hydroxytyrosol selectively kills cancer cells with minimal impact on normal cells by activating both intrinsic and extrinsic apoptotic pathways.
MMP↓, Disruption of Mitochondrial Membrane Potential
Cyt‑c↑, HT reduces mitochondrial membrane potential (ΔΨm), leading to the release of cytochrome c into the cytoplasm, activating caspase-9 and caspase-3, and triggering an apoptotic cascade (Cancer Letters, 2021).
Casp9↑,
Casp3↑,
Bcl-2↓, It downregulates anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulates pro-apoptotic proteins (Bax, Bak), promoting mitochondrial outer membrane permeabilization (MPTP opening) (Molecular Oncology, 2022).
BAX↑,
MPT↑,
Fas↑, Activation of Death Receptor-Mediated Extrinsic Apoptotic Pathway: Fas/FasL Pathway
PI3K↓, Suppression of PI3K/Akt/mTOR Pathway
Akt↓,
mTOR↓,
Mcl-1↓, decreases the expression of anti-apoptotic proteins (Mcl-1, Survivin) (Cancer Research, 2021).
survivin↓,
STAT3↓, Blockade of STAT3 Pathway
EMT↓, Hydroxytyrosol blocks key steps of tumor metastasis by regulating epithelial-mesenchymal transition (EMT), cell adhesion, invasion, and angiogenesis.
TumCI↓,
angioG↓,
E-cadherin↑, Upregulation of E-cadherin and Downregulation of N-cadherin
N-cadherin↓,
Snail↓, Inhibition of Snail/Twist Transcription Factors
Twist↓,
MMPs↓, Inhibition of Matrix Metalloproteinases (MMPs)
MMP2↓, HT downregulates the activity of MMP-2 and MMP-9, reducing extracellular matrix (ECM) degradation and inhibiting tumor cell invasion (Cancer Prevention Research, 2021).
MMP9↓,
VEGF↓, Suppression of VEGF/VEGFR Pathway
VEGFR2↓,
Hif1a↓, Degradation of HIF-1α: It inhibits the stabilization of HIF-1α under hypoxic conditions, reducing transcription of downstream pro-angiogenic genes (Molecular Cancer Therapeutics, 2021).
CSCs↓, Inhibition of Tumor Stem Cell Properties
CD44↓, Downregulation of CD44/ALDH1 Markers
Wnt↓, Inhibition of Wnt/β-catenin Pathway
β-catenin/ZEB1↓,

520-

MF,

Exposure to a 50-Hz magnetic field induced mitochondrial permeability transition through the ROS/GSK-3β signaling pathway

in-vitro,

Nor,

50 Hz, 0.4 mT, 60mins

Human amniotic epithelial cells

*MPT↑, MPT induced by MF exposure was mediated through the ROS/GSK-3β signaling pathway.
*Cyt‑c↑, induced Cyt-c release
*ROS↑, cells exposed to the MF showed increased intracellular reactive oxidative species (ROS) levels and glycogen synthase kinase-3β (GSK-3β) dephosphorylation at 9 serine residue (Ser(9))
*p‑GSK‐3β↑,
*eff↓, attenuated by ROS scavenger (N-acetyl-L-cysteine, NAC) or GSK-3β inhibitor
*MMP∅, no significant effect on mitochondrial membrane potential (ΔΨm)
*BAX↓, Bax declined around 15% which was statistically significant while the total level of Bcl-2 reminded unchanged in cells
*Bcl-2∅,

2259-

MFrot,

MF,

Method and apparatus for oncomagnetic treatment

in-vitro,

GBM,

Oncomagnetic patent

MMP↓, Oncomagnetic patent Fig 2
Bcl-2↓,
BAX↑,
Bak↑,
Cyt‑c↑,
Casp3↑, caspase staining rises progressively until after 30 min most of the cells fluoresce positive for caspase, revealing activation of this enzyme
Casp9↑,
DNAdam↑,
ROS↑, applying the oscillating magnetic field to the tissue increases the production of reactive oxygen species (ROS )
lactateProd↑,
Apoptosis↑,
MPT↑, opening of the mitochondrial membrane permeability transition pore
*selectivity↑, repetitive magnetic stimulation has shown decreased apoptosis in non -cancerous cells .
eff↑, oncomagnetic therapy may be performed in conjunction with other forms of therapy such as with chemotherapy, other forms of radiative therapy, with drugs and prescriptions, etc
MMP↓, OMF which in turn produces rapidly fluctuating or sustained depolarizations of the mitochondrial membrane potential (MMP) in the tissue .
selectivity↑, Because normal cells have a larger amount of mitochondria, have lower demand for ATP, and are not under stress, disruption of electron flow and small amount of ROS formation and MMP depolarization does not trigger apoptosis
TCA?, decrease in Krebs cycle metabolites
H2O2↑, increase in peroxide levels in GBM cells following stimulation by the system 100 using a rotating magnet
eff↑, combine the administration of BHB , or acetoacetate , or free fatty acid, or branched chain amino acid, or cryptochrome agonist , or MGMT inhibitor, or DNA alkylating agent, or DNA methylating agent, and OMF as a more effective treatment of cancer
*antiOx↑, upregulation of antioxidant mechanisms due to the application of OMFs further protects non -cancerous cells from any ROS -mediated apoptosis
H2O2↑, The experiments showed rapid increases in the levels of superoxide and H2O2 in GBM cells
eff↓, To test whether cell death is caused by the OMF - induced increase in ROS , a potent antioxidant Trolox was used to counteract it, while measuring the decrease in GBM cell count due to 4 h exposure to OMF.
GSH/GSSG↓, GSH/GSSG ratio almost exactly half that seen in control cells
*toxicity∅, No Cytotoxic Effect in Normal Cells
OS↑, OMF -Induced Prolongation of Survival in a Mouse Xenograft Model of GBM

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

 80mT pulsed

ROS↑, sOMF
mitResp↓, Inhibit Mitochondrial Respiration
mtDam↑, Produce Loss of Mitochondrial Integrity
Dose↝, Repeated intermittent sOMF was applied for 2 hours at a specific frequency, in the 200-300 Hz frequency range, with on-off epochs of 250 or 500 ms duration.
MMP?, ROS generation has been shown to be driven, in part, by elevated mitochondrial membrane chemiosmotic potential (ΔΨ) and ubiquinol (QH2)
OCR↓, Immediately after cessation of field rotation we observe a loss of mitochondrial integrity (labeled LMI), with a very rapid increase in O2 consumption
mt-H2O2↑, We have previously demonstrated that sOMF treatment of cells generates superoxide/hydrogen peroxide in the mitochondrial matrix
eff↓, we repeated the same experiment in the presence of Trolox, which protects thiols from ROS oxidation (47). sOMF treatment of RLM in State 3u pre-treated with Trolox (15 μM), show minimal inhibition,
SDH↓, SDH Inhibition by sOMF in State 3u RLM Is Caused by ROS Generation
Thiols↓, suggest that thiol oxidation in SDH may result from sOMF.
GSH↓, Glutathione in the mitochondrial matrix can provide some protection from ROS, but after solubilizing the mitochondria, this protection is lost and the SDH becomes more sensitive to sOMF.
TumCD↑, sOMF is highly effective at killing non-dividing GBM cell cultures,
Casp3↑, caspase-3 activation 1 h after sOMF
Casp7↑, rapid activation of caspase-3/7
MPT↑, OMF-treated cell that causes near simultaneous MPT, release of cytochrome c and other apoptosis-inducing factors, resulting in caspase-3/7 activation in these GBM cells.
Cyt‑c↑,
selectivity↑, differential sensitivity to sOMF of cancer cells over ‘normal’ cells becomes apparent. rapid increase in the reactive oxygen species (ROS) in the mitochondria to cytotoxic levels only in cancer cells, and not in normal human cortical neurons
GSH/GSSG↓, increasing GSSG/GSH ratio
ETC↓, completely arrest electron transport in isolated, respiring, rat liver mitochondria and patient derived glioblastoma (GBM)

5609-

NaHCO3,

Alkalization of cellular pH leads to cancer cell death by disrupting autophagy and mitochondrial function

in-vitro,

Var,

eff↑, We then reported that alternate infusion of bicarbonate and anticancer agent into tumors via tumor feeding artery markedly enhanced the efficacy of transarterial chemoembolization (TACE) in the local control of hepatocellular carcinoma (HCC).
e-pH↑, Alkalizing cellular pH by bicarbonate decreased pH gradient (ΔpH), membrane potential (ΔΨm), and proton motive force (Δp) across the inner membrane of mitochondria;
MMP↓,
OXPHOS↝, disruption of oxidative phosphorylation (OXPHOS) due to collapsed Δp
AMP↑, led to a significant increase in adenosine monophosphate (AMP), which activated the classical AMPK-mediated autophagy.
TumAuto↑,
MPT↑, Bicarbonate also induced persistent mitochondrial permeability (MPT) and damaged mitochondria.
mtDam↑,

Showing Research Papers: 1 to 16 of 16

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 16

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 3, ROS↓, 1, ROS↑, 1,

Mitochondria & Bioenergetics ⓘ

MMP∅, 1, MPT↑, 1,

Cell Death ⓘ

BAX↓, 1, Bcl-2∅, 1, Cyt‑c↑, 1, TRPV1↑, 1,

Proliferation, Differentiation & Cell State ⓘ

p‑GSK‐3β↑, 1,

Migration ⓘ

Ca+2↑, 1,

Barriers & Transport ⓘ

BBB↓, 1,

Immune & Inflammatory Signaling ⓘ

Imm↑, 1, Inflam↓, 1,

Protein Aggregation ⓘ

Aβ↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↑, 1, BioAv↝, 1, eff↓, 1, Half-Life↓, 1, selectivity↑, 1,

Clinical Biomarkers ⓘ

GutMicro↑, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, cardioP↑, 1, neuroP↑, 1, toxicity∅, 1,
Total Targets: 26

Scientific Paper Hit Count for: MPT, mitochondrial permeability transition

3 Capsaicin
3 Magnetic Fields
2 Curcumin
2 Magnetic Field Rotating
1 3-bromopyruvate
1 Silver-NanoParticles
1 alpha Linolenic acid
1 Carvacrol
1 Thymol-Thymus vulgaris
1 Celecoxib
1 chitosan
1 methylseleninic acid
1 HydroxyTyrosol
1 Bicarbonate(Sodium)

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#:%  Target#:519  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

MPT Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Cell Death ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Home Page