MMP Cancer Research Results

MMP, ΔΨm, mitochondrial membrane potential: Click to Expand ⟱
Source:
Type:
Destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis.
Mitochondria are organelles within eukaryotic cells that produce adenosine triphosphate (ATP), the main energy molecule used by the cell. For this reason, the mitochondrion is sometimes referred to as “the powerhouse of the cell”.
Mitochondria produce ATP through process of cellular respiration—specifically, aerobic respiration, which requires oxygen. The citric acid cycle, or Krebs cycle, takes place in the mitochondria.
The mitochondrial membrane potential is widely used in assessing mitochondrial function as it relates to the mitochondrial capacity of ATP generation by oxidative phosphorylation. The mitochondrial membrane potential is a reliable indicator of mitochondrial health.
In cancer cells, ΔΨm is often decreased, which can lead to changes in cellular metabolism, increased glycolysis, increased reactive oxygen species (ROS) production, and altered cell death pathways.

The membrane of malignant mitochondria is hyperpolarized (−220 mV) in comparison to their healthy counterparts (−160 mV), which facilitates the penetration of positively charged molecules to the cancer cells mitochondria.
The MMP is a critical indicator of mitochondrial function, directly reflecting the organelle's capacity to generate ATP through oxidative phosphorylation.


Scientific Papers found: Click to Expand⟱
2023- BBR,    Berberine Induces Caspase-Independent Cell Death in Colon Tumor Cells through Activation of Apoptosis-Inducing Factor
- in-vitro, Colon, NA - in-vitro, Nor, YAMC
TumCD↑, Berberine decreased colon tumor colony formation in agar, and induced cell death and LDH release in a time- and concentration-dependent manner in IMCE cells.
*toxicity↓, In contrast, YAMC(normal) cells were not sensitive to berberine-induced cell death. less cytotoxic effects on normal colon epithelial cells.
selectivity↑, see figure 2
ROS↑, berberine-stimulated ROS production
*ROS∅, ROS production in a concentration-dependent manner only in IMCE cells, but not in YAMC cells. In YAMC cells, berberine did not induce ROS production
MMP↓, berberine induced mitochondrial depolarization in a concentration-dependent manner in IMCE cells, but not in YAMC cells
*MMP∅, but not in YAMC cells
PARP↑, Berberine Activation of PARP
BioAv↝, absorption of berberine by YAMC is lower than that by IMCE cells

1264- CAP,    Capsaicin modulates proliferation, migration, and activation of hepatic stellate cells
- in-vitro, HCC, NA
TumCP↓,
TumCMig↓,
TumCCA↑, G0/G1 cell cycle arrest
MMP∅, Capsaicin did not provoke significant loss of MMP
MMP2↓,
MMP9↓,
α-SMA↓,
COL1A1↓,
COL3A1↓,
TIMP1↓,

2019- CAP,    Capsaicin: A Two-Decade Systematic Review of Global Research Output and Recent Advances Against Human Cancer
- Review, Var, NA
chemoPv↑, Capsaicin has shown significant prospects as an effective chemopreventive agent
Ca+2↑, Capsaicin was shown to cause upstream activation of Ca2+
antiOx↑, Another plausible mechanism implicated in the chemopreventive action of capsaicin is its anti-oxidative effects.
*ROS↓, capsaicin inhibits ROS release and the subsequent mitochondrial membrane potential collapse, cytochrome c expression, chromosome condensation, and caspase-3 activation induced by oxidized low-density lipoprotein in normal human HUVEC cells
*MMP∅,
*Cyt‑c∅,
*Casp3∅,
*eff↑, dietary curcumin and capsaicin concurrent administration in high-fat diet-fed rats were shown to mitigate the testicular and hepatic antioxidant status by increasing GSH levels, glutathione transferase activity, and Cu-ZnSOD expression
*Inflam↓, Anti-inflammation is another mechanism implicated in the chemopreventive action of capsaicin.
*NF-kB↓, inhibition of NF-kB by capsaicin
*COX2↓, compound elicits COX-2 enzyme activity inhibition and downregulation of iNOS
iNOS↓,
TRPV1↑, major pro-apoptotic mechanisms of capsaicin is via the vanilloid receptors, primarily TRPV1
i-Ca+2?, causing a concomitant influx of Ca2+: severe condition of mitochondria calcium overload. at high concentration (> 10 µM), capsaicin induces a slow but persistent increase in intracellular Ca2+
MMP↓, depolarization of mitochondria membrane potential
Cyt‑c↑, release of cytochrome C
Bax:Bcl2↑, activation of Bax and p53 through C-jun N-terminal kinase (JNK) activation
P53↑,
JNK↑,
PI3K↓, blocking the Pi3/Akt/mTOR signalling pathway, capsaicin increases levels of autophagic markers (LC3-II and Atg5)
Akt↓,
mTOR↓,
LC3II↑,
ATG5↑,
p62↑, enhances p62 and Fap-1 degradation and increases caspase-3 activity to induce apoptosis in human nasopharyngeal carcinoma cells
Fap1↓,
Casp3↑,
Apoptosis↑,
ROS↑, generation of ROS in human hepatoma (HepG2 cells)
MMP9↓, inhibition of MMP9 by capsaicin occurs via the suppression of AMPK-NF-κB, EGFR-mediated FAK/Akt, PKC/Raf/ERK, p38 MAPK, and AP-1 signaling pathway
eff↑, capsaicin 8% patch could promote the regeneration and restoration of skin nerve fibres in chemotherapy-induced peripheral neuropathy in addition to pain relief
eff↓, capsaicin has shown several unpleasant side effects, including stomach cramps, skin and gastric irritation, and burning sensation
eff↑, liposomes and micro-emulsion-based drugs have been known to significantly improve oral bioavailability and reduce the irritation of drugs
selectivity↑, In addition, these delivery systems can be surfaced-modified to perform site-directed/cell-specific drug delivery, thereby ensuring increased cell death of cancer cells while sparing non-selective normal cells
eff↑, Furthermore, owing to its antioxidant potential, capsaicin has been applied as a bioreduction and capping agent to synthesize biocompatible silver nanoparticles
ChemoSen↑, capsaicin has been combined with other anticancer therapies for more pronounced anticancer effects

6082- CHOC,    Potential for preventive effects of cocoa and cocoa polyphenols in cancer
- Review, Var, NA
*ROS↓, Cocoa flavonoids have been demonstrated to influence several important biological functions in vitro and in vivo by their free radical scavenging ability
Apoptosis↑, or through the regulation of signal transduction pathways to stimulate apoptosis and to inhibit inflammation, cellular proliferation, apoptosis, angiogenesis and metastasis.
Inflam↓,
TumCP↓,
angioG↓,
TumMeta↓,
*Ca+2↓, oxidative stress in lead-exposed cells through the downregulation of ROS generation, decrease of intracellular calcium and prevented the alteration of the mitochondrial membrane potential
*MMP∅,
CYP1A1↑, A polyphenolic cocoa extract increased CYP1A1 mRNA and protein levels and enzymatic activity in MCF-7 and SKBR3 breast cancer cells
PGE2↓, Cocoa phenolic extract inhibited the inflammatory mediator prostaglandin E2 in human intestinal Caco-2 cells
TumCCA↑, Cocoa-derived pentameric procyanidin (pentamer) caused G0/G1 cell cycle arrest in human breast cancer MDA MB-231,
chemoPv↑, This study demonstrated that a co- coa-rich diet could prevent the early stage of chemically induced colorectal cancer in rats

850- Gra,    Selective cytotoxic and anti-metastatic activity in DU-145 prostate cancer cells induced by Annona muricata L. bark extract and phytochemical, annonacin
- in-vitro, PC, PC3 - in-vitro, Pca, DU145
ROS∅, EAB extract and annonacin does not elicit ROS generation in DU-145 cells
MMP∅,
Casp3↑, suggesting a caspase independent cell death
Casp7↑,
VEGF↓,

520- MF,    Exposure to a 50-Hz magnetic field induced mitochondrial permeability transition through the ROS/GSK-3β signaling pathway
- in-vitro, Nor, NA
*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∅,

2057- PB,    Trichomonas vaginalis induces apoptosis via ROS and ER stress response through ER–mitochondria crosstalk in SiHa cells
- in-vitro, Cerv, SiHa
ROS↓, Pretreatment with N-acetyl cysteine (ROS scavenger) or 4-phenylbutyric acid (4-PBA; ER stress inhibitor) significantly alleviated apoptosis, mitochondrial ROS production, mitochondrial dysfunction and ER stress response in a dose-dependent manner.
tumCV∅, There was no difference in cell viability between the SiHa cells treated with 2 mM 4-PBA for 6 h and cell in the untreated control group
cl‑PARP↓, Surprisingly, 4-PBA pretreatment attenuated the levels of cleaved PARP and caspase-3 in T. vaginalis-infected SiHa cells in a dose-dependent manner
cl‑Casp3↓,
MMP∅, T. vaginalis induced MMP depolarization in the SiHa cells; however, these changes in fluorescence were suppressed by 4-PBA pretreatment
ER Stress↓, pretreatment with the ER stress inhibitor 4-PBA was found to significantly attenuate the levels of ER stress-related proteins in T. vaginalis-infected cells


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 ⓘ

antiOx↑, 1,   CYP1A1↑, 1,   ROS↓, 1,   ROS↑, 2,   ROS∅, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 2,   MMP∅, 3,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   Bax:Bcl2↑, 1,   Casp3↑, 2,   cl‑Casp3↓, 1,   Casp7↑, 1,   Cyt‑c↑, 1,   Fap1↓, 1,   iNOS↓, 1,   JNK↑, 1,   TRPV1↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics ⓘ

tumCV∅, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   LC3II↑, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,   PARP↑, 1,   cl‑PARP↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,   PI3K↓, 1,  

Migration ⓘ

Ca+2↑, 1,   i-Ca+2?, 1,   COL1A1↓, 1,   COL3A1↓, 1,   MMP2↓, 1,   MMP9↓, 2,   TIMP1↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   PGE2↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   ChemoSen↑, 1,   eff↓, 1,   eff↑, 3,   selectivity↑, 2,  

Functional Outcomes ⓘ

chemoPv↑, 2,  
Total Targets: 51

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

ROS↓, 2,   ROS↑, 1,   ROS∅, 1,  

Mitochondria & Bioenergetics ⓘ

MMP∅, 4,   MPT↑, 1,  

Cell Death ⓘ

BAX↓, 1,   Bcl-2∅, 1,   Casp3∅, 1,   Cyt‑c↑, 1,   Cyt‑c∅, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑GSK‐3β↑, 1,  

Migration ⓘ

Ca+2↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 18

Scientific Paper Hit Count for: MMP, ΔΨm, mitochondrial membrane potential
2 Capsaicin
1 Berberine
1 Chocolate
1 Graviola
1 Magnetic Fields
1 Phenylbutyrate
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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