MOMP Cancer Research Results

MOMP, Mitochondrial Outer Membrane Permeabilization: Click to Expand ⟱
Source:
Type:
MOMP is the point-of-no-return decision step of intrinsic apoptosis. It is the event in which the mitochondrial outer membrane becomes permeable, allowing release of pro-death factors that irreversibly commit a cell to die. Cancer progression is characterized by systematic suppression, buffering, or decoupling of MOMP from lethal execution.

MOMP occurs when BAX and/or BAK oligomerize in the mitochondrial outer membrane, forming pores that release:
-Cytochrome c → apoptosome → caspase-9
-Smac/DIABLO → IAP neutralization
-Other apoptogenic factors (e.g., Omi/HtrA2)
Once sufficient mitochondria undergo MOMP, cell death is inevitable (even if caspases are later inhibited).
Redox, Metabolism, and MOMP (Critical)
-High xCT / GSH → suppress mitochondrial ROS → MOMP ↓
-Autophagic flux → removes damaged mitochondria → MOMP ↓
-Pro-oxidant overload → mitochondrial dysfunction → MOMP ↑


Scientific Papers found: Click to Expand⟱
5378- ART/DHA,    Natural Agents Modulating Ferroptosis in Cancer: Molecular Pathways and Therapeutic Perspectives
- Review, Var, NA
Ferroptosis↑, Artemisinin increases ferroptosis risk in cancer cells by increasing cellular free iron and lipid peroxidation, causing increased membrane permeability and decreased integrity [59]
Iron↑,
lipid-P↑,
MOMP↑,
AntiCan↑, Artemisinin has anticancer and antimalarial properties by upregulating NCOA4 and DMT1 levels, raising ferrous ion levels, and causing ferroptosis by downregulating GSH and GPX4 levels [30, 59, 75].
NCOA4↑,
GSH↓,
GPx4↓,
ROS↑, Artemisinin and its derivatives regulate 20 iron metabolism genes, thereby causing the formation of ROS [76]
ChemoSen↑, Artesunate, when combined with sorafenib, can enhance the susceptibility of hepatocellular carcinoma cells to cisplatin resistance through ferroptosis inhibition [77].
ER Stress↑, artemisinin, specifically ferroptosis, by controlling iron metabolism, producing ROS, and triggering ER‐stress.
DNAdam↑, primary antineoplastic mechanisms of artemisinin are ferroptosis, DNA damage, tumour angiogenesis suppression and cell cycle inhibition [78]
angioG↓,
TumCCA↑,
eff↓, while NAC and ferrostatin‐1 partially reverse these effects [82]

5130- ART/DHA,    Dihydroartemisinin Induces Apoptosis in Human Bladder Cancer Cell Lines Through Reactive Oxygen Species, Mitochondrial Membrane Potential, and Cytochrome C Pathway
- in-vitro, Bladder, T24/HTB-9
tumCV↓, DHA significantly reduced cell viability in a dose-dependent manner.
eff↓, Cytotoxicity of DHA was suppressed by N-acetylcysteine (NAC)
Apoptosis↑, induction of cell apoptosis, which were manifested by annexin V-FITC staining, activation of caspase-3
Casp3↑,
ROS↑, DHA also increased ROS generation, cytochrome c release, and loss of mitochondrial transmembrane potential (ΔΨm) in cells.
Cyt‑c↑,
MMP↓,
Bcl-2↓, downregulation of regulatory protein Bcl-2 and upregulation of Bax protein by DHA were also observed
BAX↑,
MOMP↑, Dihydroartemisinin increases mitochondrial permeability of EJ-138 and HTB-9 cells by Collapse of ΔΨm
TumCG↓, It has shown that DHA selectively inhibits the growth of many cancer cells types, such as leukemia,[29] pancreas,[30] breast[31] and prostate[32] cancers

6350- DRE,    Tracking Evidences of Dandelion for the Treatment of Cancer: From Chemical Composition, Bioactivity, Signaling Pathways in Cancer Cells to Perspective Study
- Review, Var, NA
AntiCan↑, Dandelion, one of the important medicinal and edible plants, is effective in anticancer, inhibition of bacterial growth, hypoglycemic, and anti-inflammation, as well as antioxidant.
*Bacteria↓,
*Inflam↓,
*antiOx↑,
TumCCA↑, Cell Cycle Arrest and Anti-Proliferation in Cancer Cells
Apoptosis↑, Induction of Cell Apoptosis in Cancer Cells
MOMP↑, increased permeability of the outer mitochondrial membrane and mediating the release of cytochrome c (Cyt-c).
Cyt‑c↑,
APAF1↑, activating factor-1 (Apaf-1) and cystein asparate protease-9 (Caspase-9)
Casp9↑,
Casp3↑, then activates Caspase-3 to trigger the Caspase cascade reaction and induce cell apoptosis.
MMP↓, disrupting mitochondrial membrane potential, activating Caspase-9 and Caspase-3, and downregulating the expression of Bcl-2 in human breast cancer MDA-MB-231
Bcl-2↓,
TumCMig↓, Inhibition of Migration and Invasion of Cancer Cells
TumCI↓,
Wnt↓, taraxasterol inhibits the migration and invasion of human thyroid papillary carcinoma TPC-1 and BCPAP cells by regulating Wnt/β-catenin signaling and suppressing the expression of MMP-2 and MMP-9
β-catenin/ZEB1↓,
MMP2↓,
MMP9↓,
TumAuto↑, Induction of Autophagy in Cancer Cells
mTOR↓, inhibiting the mTOR/ eukaryotic translation initiation factor 4E binding protein 1 (4EBP1) pathway.
4E-BP1↓,
Glycolysis↓, Taraxasterol significantly reduces the level of glyceraldehyde-3-phosphate dehydrogenase in aerobic glycolysis,
angioG↓, Anti-Angiogenesis in Cancer Cells

6367- DRE,    Antioxidant and antimicrobial activities of Dandelion root extract (Taraxacum officinale) and its cytotoxic effect on MDA-MB-231 breast cancer cells
- in-vitro, BC, MDA-MB-231
TumCD↑, Our study indicates that DRE has proven novel in killing breast cancer cells, has a mildly vigorous antioxidant activity to scavenge free radicals,
*antiOx↑,
*ROS↓,
tumCV↓, fig 3
Apoptosis↑, dandelion root can cause apoptosis in MDA-MB-231 cells, that DRE has antioxidant properties against reactive oxygen species
ROS↑, The degradation of the breast cancer cells might be due to the presence of ROS groups and the action of some bioactive compounds like polyphenols and triterpenoids in the extract.
TumCCA↑, DRE through G2/M cell cycle arrest and alteration in the amino acids (Figs. 5, 6) that make up the endoplasmic reticulum
MOMP↑, The DRE penetrates the outer membrane, causing ROS to disrupt the mitochondria, breakage of the double strand in the DNA
ROS↑,

5519- EP,    Nanosecond Pulsed Electric Fields (nsPEFs) for Precision Intracellular Oncotherapy: Recent Advances and Emerging Directions
- Review, Var, NA
MMP↓, nsPEF bypasses plasma-membrane shielding to porate organelles, collapse mitochondrial potential, perturb ER calcium, and transiently open the nuclear envelope.
Ca+2↑,
eff↑, synergy with checkpoint blockade.
ER Stress↑, capacity to directly target organelles such as mitochondria, endoplasmic reticulum (ER),
selectivity↑, selectively ablate solid tumors, suppress metastatic spread, and prime systemic anti-tumor immunity while sparing adjacent normal tissue [7,9,10,11,12,13,14,15].
CSCs↓, Preclinical investigations have demonstrated that nsPEFs significantly reduce CSC-associated subpopulations, including CD44+/CD24− cells in breast cancer xenografts and CD133+ glioma stem-like cells
CD44↓,
CD133↓,
ROS↑, nsPEFs release Ca2+ from the ER, disrupt mitochondrial membrane potential, induce reactive oxygen species (ROS) generation, and perturb nuclear chromatin structure within nanoseconds
Imm↑, nsPEFs not only eliminate local tumor cells but also convert the tumor into an in situ vaccine, amplifying their therapeutic relevance in the era of immunotherapy
DNAdam↑, figure 2
MOMP↑, induce mitochondrial outer membrane permeabilization (MOMP)
Cyt‑c↑,
Casp9↑, Subsequent release of cytochrome c enables apoptosome assembly, caspase-9 activation, and downstream activation of caspases-3/7, culminating in cell death
Casp3↑,
Casp9↑,
TumCD↑,
Fas↑, In certain cell types, nsEP can also activate the extrinsic pathway, where Fas receptor clustering stimulates caspase-8.
UPR↑, This rapid surge triggers ER stress pathways, activates unfolded protein response (UPR) signaling, and promotes cross-talk with mitochondria through mitochondria-associated membranes (MAMs)
Dose↝, longer ns pulses (100–300 ns) generate sustained plasma membrane charging, resulting in robust Ca2+ influx, osmotic imbalance, and apoptotic priming.
Dose↝, A critical threshold of 10–20 kV/cm is generally required to initiate pore formation in malignant cells, with higher amplitudes (>30–40 kV/cm) producing more extensive permeabilization [100].
Dose↓, Low pulse counts (<100) frequently produce reversible stress responses, such as transient mitochondrial depolarization or ER Ca2+ release, without committing cells to apoptosis. I
Dose↑, In contrast, higher pulse counts (500–1000) lead to irreversible apoptosis, caspase activation, and release of DAMPs that initiate ICD [80,106].
HMGB1↓, ICD after nsPEF is characterized by surface exposure of calreticulin, extracellular ATP release, and HMGB1 emission
eff↑, The integration of nsPEFs with NP-based systems thus represents a synergistic platform where physical membrane poration and molecular targeting cooperate to maximize therapeutic efficacy.
EPR↑, demonstrates that PEF + AuNPs enhanced membrane permeabilization compared with PEF alone,
ChemoSen↑, The superior efficacy of delayed drug administration following nsPEF exposure can be attributed to transient biophysical and biochemical changes that persist after pulsing.
ETC↝, study demonstrated that nsPEFs dynamically alter trans-plasma membrane electron transport (tPMET) and mitochondrial electron transport chain activity, resulting in differential ROS generation in cancer versus non-cancer cells (Figure 9).
*AntiAge↑, Mechanistically, nsPEFs upregulated HIF-1α and SIRT1, mediators of mitochondrial retrograde signaling, thereby reversing hallmarks of aging
*Hif1a↑,
*SIRT1↑,

6487- Nimb,    Anticancer properties of nimbolide and pharmacokinetic considerations to accelerate its development
- Review, Var, NA
TumCP↓, anti-proliferation, induction of apoptosis, inhibition of metastasis and angiogenesis, and modulation of carcinogen-metabolizing enzymes.
Apoptosis↓,
TumMeta↑,
angioG↓,
*antiOx↑, nimbolidehas been found to possess antioxidant effect and free radical scavenging activities.
*eff↑, In comparison to azadirachtin and ascorbic acid (vitamin C), nimbolide was shown to be a more potent antioxidant
Apoptosis↑, Nimbolide induces apoptosis through diverse molecular mechanism(s).
MOMP↑, Nimbolide disrupts MOMP, which promotes caspases activation leading to apoptosis.
CDK1↓, Nimbolide also reduces the level of CDKs and cyclins, causing cell cycle arrest.
TumCCA↑,
MAPK↓, Nimbolide also abrogates various signaling cascades including MAPK (ERK1/2), JAK2/STAT3 and PI3K/Akt, leading to suppression of proliferation of a wide variety of human cancer cells.
JAK2↓,
STAT3↓,
PI3K↓,
Akt↓,
TumCP↓,
*NRF2↑, Nimbolide disrupts the Nrf2-KEAP1 complex and promotes the release of Nrf2, thus increasing levels of antioxidant and detoxification enzymes.
NF-kB↓, Inhibition of the NF-κB pathway also reduces the dissociation of GSK-3β from β-catenin, hence restraining the Wnt/β-catenin
GSK‐3β↑,
Wnt↓,
β-catenin/ZEB1↓,
chemoPv↑, nimbolide showed remarkable chemopreventive property.
Bcl-xL↓, Nimbolide treatmentdecreased the expression of antiapoptotic proteins(Bcl-xL, Bcl-2, survivin, caspase inhibitor molecules) and increased the expression of proapoptotic proteins (cytochrome c, Bax, Bad, Bid, cleaved caspases) in prostate cancer cells
Bcl-2↓,
survivin↓,
Cyt‑c↑,
BAX↑,
BID↑,
cl‑Casp↑,
P53↑, nimbolide acted by up-regulation of p53 levelin HeLa cells, thereby priming these cells towards apoptosis by destabilizing the mitochondria
DR5↑, Nimbolide up-regulated the expression of both DR5 and DR4 in chronic myeloid leukemia (KBM-5), multiple myeloma (U266), embryonic kidney carcinoma (A293), pancreatic adenocarcinoma (AsPC-1), and breast adenocarcinoma (MDA-MB-231) cells
DR4↑,
ROS↑, nimbolide resulted in generation of reactive oxygen species (ROS)
lipid-P↑, ROS also induced lipid peroxidation of cellular membranes, generating toxic metabolites such as malondialdehyde (MDA) that can react with DNA to form adducts to induce apoptosis.
MDA↑,
MMP2↓, nimbolide reduced mRNA expression of MMP-2, MMP-9, uPA and uPA receptor in breast cancer cells (MCF-7)
MMP9↓,
uPA↓,
ICAM-1↓, nimbolide was shown to downregulate the expression of MMP-9, ICAM-1, and CXCR4 in colorectal cancer xenografts
CXCR4↓,
CXCR2↓, nimbolide also reduced expression of CXCL8 and CXCR2 in breast cancers, and thus abrogated angiogenesis
angioG↓,
BBB↑, nimbolide might be able to cross blood-brain barrier (BBB) and the concentration could be sufficient for nimbolide to suppress intracranial tumour cell proliferation.

5125- Sal,    Salinomycin induced ROS results in abortive autophagy and leads to regulated necrosis in glioblastoma
- in-vitro, GBM, NA
ER Stress↑, SLM induces a potent endoplasmic reticulum (ER) stress followed by the trigger of the unfolded protein response (UPR) and an aberrant autophagic flux that culminated in necrosis due to mitochondria and lysosomal alterations.
UPR↑,
autoF↓, SLM treatment does not trigger apoptosis and blocks the autophagy flux in glioma cell line
lysosome↝,
ROS↑, aberrant autophagic flux was orchestrated by the production of Reactive Oxygen Species (ROS)
lipid-P↑, our data suggest that in our system the oxidative stress blocks the autophagic flux through lipid oxidation.
CSCs↓, SLM induces a potent antitumor effect in brain tumor stem cells (BTSCs) and established adult and pediatric glioma cell lines in vitro
necrosis↑, SLM induces necrosis cell death
ATP↓, with increasing doses of SLM displayed a decrease in intracellular ATP levels
MMP↓, SLM treated cells displayed significantly lower ΔΨm than untreated cells
MOMP↑, SLM induces mitochondrial MOMP.
DNAdam↑, We observed double strand breaks in SLM-treated cells (Figure 4C) and it is possible that this DNA damage is induced as a consequence of AIF internalization.
AIF↑,
lysoMP↑, hypothesis that SLM treatment triggers an autophagic process that cannot proceed adequately because of LMP resulting from oxidative stress.
MitoP↑, In addition, impairment of mitochondrial activity would trigger mitophagy, with engulfment of the organelle and initiation of autophagy.
Ca+2↑, The elevated levels of calcium and ROS inside mitochondria results in MOMP


Showing Research Papers: 1 to 7 of 7

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

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   Iron↑, 1,   lipid-P↑, 3,   MDA↑, 1,   ROS↑, 7,  

Metal & Cofactor Biology(tgid=2) ⓘ

NCOA4↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

AIF↑, 1,   ATP↓, 1,   ETC↝, 1,   MMP↓, 4,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Glycolysis↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   APAF1↑, 1,   Apoptosis↓, 1,   Apoptosis↑, 4,   BAX↑, 2,   Bcl-2↓, 3,   Bcl-xL↓, 1,   BID↑, 1,   cl‑Casp↑, 1,   Casp3↑, 3,   Casp9↑, 3,   Cyt‑c↑, 4,   DR4↑, 1,   DR5↑, 1,   Fas↑, 1,   Ferroptosis↑, 1,   lysoMP↑, 1,   MAPK↓, 1,   MOMP↑, 7,   necrosis↑, 1,   survivin↓, 1,   TumCD↑, 2,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 2,  

Protein Folding & ER Stress(tgid=8) ⓘ

ER Stress↑, 3,   UPR↑, 2,  

Autophagy & Lysosomes(tgid=9) ⓘ

autoF↓, 1,   lysosome↝, 1,   MitoP↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 3,   P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↓, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

4E-BP1↓, 1,   CD133↓, 1,   CD44↓, 1,   CSCs↓, 2,   GSK‐3β↑, 1,   mTOR↓, 1,   PI3K↓, 1,   STAT3↓, 1,   TumCG↓, 1,   Wnt↓, 2,  

Migration(tgid=13) ⓘ

Ca+2↑, 2,   MMP2↓, 2,   MMP9↓, 2,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↑, 1,   uPA↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 4,   EPR↑, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CXCR2↓, 1,   CXCR4↓, 1,   HMGB1↓, 1,   ICAM-1↓, 1,   Imm↑, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 2,   Dose↓, 1,   Dose↑, 1,   Dose↝, 2,   eff↓, 2,   eff↑, 2,   selectivity↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   chemoPv↑, 1,  
Total Targets: 84

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   NRF2↑, 1,   ROS↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SIRT1↑, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 9

Scientific Paper Hit Count for: MOMP, Mitochondrial Outer Membrane Permeabilization
2 Artemisinin
2 Dandelion Root
1 Electrical Pulses
1 Nimbolide
1 salinomycin
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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