MMP9 Cancer Research Results
MMP9, MMP9: Click to Expand ⟱
| Source: HalifaxProj(suppress) |
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Matrix metalloproteinase-9 (MMP-9) is an enzyme that plays a significant role in the degradation of extracellular matrix components.
MMP-9 facilitates the breakdown of the extracellular matrix, which can enable cancer cells to invade surrounding tissues and spread to distant sites (metastasis).
Elevated levels of MMP-9 have been associated with poor prognosis in several cancers, including breast, lung, and colorectal cancers.
MMP2 and MMP9: two enzymes are critical to tumor invasion.
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Scientific Papers found: Click to Expand⟱
EPR↝, takes advantage of EPR
ROS↑, silver ions drive the formation of ROS, which triggers massive oxidative stress, thereby activating the cellular pathways leading to cell death
IL1↑, IL-1b
IL8↑, IL-8 mRNA levels
ER Stress↑,
MMP9↑, it has been shown that 20 nm AgNPs increase the MMP-9 secretion
MMP↓, loss of mitochondrial membrane potential and mitochondrial structural disorganization, were reported to accompany the AgNP-induced stres
Cyt‑c↑, cytochrome c release from the mitochondria into the cytoplasm and finally to apoptosis
Apoptosis↑,
Hif1a↑, AgNPs were shown to induce HiF-1α activation, thereby ultimately activating autophagy through the AMPK-mTOR pathway in PC-3 prostate cancer cells [89
BBB↑, AgNPs can affect the integrity of the blood–brain barrier and can cross this barrier in vitro through transcytosis
GutMicro↝, AgNP treatments might influence the composition of the gut microbiota,
eff↑, AgNPs are promising tools for targeted delivery
eff↑, the joint application of the nanoparticles and the HDAC inhibitor caused significantly increased ROS levels,
RadioS↑, idea to use AgNPs as radiosensitizers came along with the phenomenon that metals with high atomic numbers are capable of enhancing the effects of radiation
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in-vitro, |
Colon, |
SW480 |
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in-vitro, |
Colon, |
CT26 |
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TumCP↓, high-concentration of capsaicin (≥ 200 µM for SW480 and CT-26 cell lines; ≥ 25 µM for HCT116 cell line) inhibited CRC cell proliferation in a dose-dependent manner
TumCMig↑, low-concentration of capsaicin (100 µM for SW480 and CT-26 cell lines; 12.5 µM for HCT116 cell line) enhanced both migratory and invasive capability of these cells
TumCI↑,
EMT↑, 100 µM capsaicin induced epithelial-to-mesenchymal (EMT), up-regulated expression of MMP-2 and MMP-9, and activated Akt/mTOR and STAT-3 pathways in SW480 cells.
MMP2↓,
MMP9↑,
STAT3↑,
TumMeta↑, capsaicin-induced metastasis of CRC cells was mediated by modulating reactive oxygen species (ROS) production.
ROS↑,
PI3K↓, It can block Phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling in different animals against various cancers
Akt↓,
mTOR↓,
MMP9↑, Chrysin strongly suppresses Matrix metalloproteinase-9 (MMP-9), Urokinase plasminogen activator (uPA) and Vascular endothelial growth factor (VEGF), i.e. factors that can cause cancer
uPA↓,
VEGF↓,
AR↓, Chrysin has the ability to suppress the androgen receptor (AR), a protein necessary for prostate cancer development and metastasis
Casp↑, starts the caspase cascade and blocks protein synthesis to kill lung cancer cells
TumMeta↓, Chrysin significantly decreased lung cancer metastasis i
TumCCA↑, Chrysin induces apoptosis and stops colon cancer cells in the G2/M cell cycle phase
angioG↓, Chrysin prevents tumor growth and cancer spread by blocking blood vessel expansion
BioAv↓, Chrysin’s solubility, accessibility and bioavailability may limit its medical use.
*hepatoP↑, As chrysin reduced oxidative stress and lipid peroxidation in rat liver cells exposed to a toxic chemical agent.
*neuroP↑, Protecting the brain against oxidative stress (GPx) may be aided by increasing levels of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx).
*SOD↑,
*GPx↑,
*ROS↓, A decrease in oxidative stress and an increase in antioxidant capacity may result from chrysin’s anti-inflammatory properties
*Inflam↓,
*Catalase↑, Supplementation with chrysin increased the activity of antioxidant enzymes like SOD and catalase and reduced the levels of oxidative stress markers like malondialdehyde (MDA) in the colon tissue of the rats.
*MDA↓, Antioxidant enzyme activity (SOD, CAT) and oxidative stress marker (MDA) levels were both enhanced by chrysin supplementation in mouse liver tissue
ROS↓, reduction of reactive oxygen species (ROS) and oxidative stress markers in the cancer cells further indicated the antioxidant activity of chrysin
BBB↑, After crossing the blood-brain barrier, it has been shown to accumulate there
Half-Life↓, The half-life of chrysin in rats is predicted to be close to 2 hours.
BioAv↑, Taking chrysin with food may increase the effectiveness of the supplement: increased by a factor of 1.8 when taken with a high-fat meal
ROS↑, In contrast to 5-FU/oxaliplatin, chrysin increases the production of reactive oxygen species (ROS), which in turn causes autophagy by stopping Akt and mTOR from doing their jobs
eff↑, mixture of chrysin and cisplatin caused the SCC-25 and CAL-27 cell lines to make more oxygen free radicals. After treatment with chrysin, cisplatin, or both, the amount of reactive oxygen species (ROS) was found to have gone up.
ROS↑, When reactive oxygen species (ROS) and calcium levels in the cytoplasm rise because of chrysin, OC cells die.
ROS↑, chrysin is the cause of death in both types of prostate cancer cells. It does this by depolarizing mitochondrial membrane potential (MMP), making reactive oxygen species (ROS), and starting lipid peroxidation.
lipid-P↑,
ER Stress↑, when chrysin is present in DU145 and PC-3 cells, the expression of a group of proteins that control ER stress goes up
NOTCH1↑, Chrysin increased the production of Notch 1 and hairy/enhancer of split 1 at the protein and mRNA levels, which stopped cells from dividing
NRF2↓, Not only did chrysin stop Nrf2 and the genes it controls from working, but it also caused MCF-7 breast cancer cells to die via apoptosis.
p‑FAK↓, After 48 hours of treatment with chrysin at amounts between 5 and 15 millimoles, p-FAK and RhoA were greatly lowered
Rho↓,
PCNA↓, Lung histology and immunoblotting studies of PCNA, COX-2, and NF-B showed that adding chrysin stopped the production of these proteins and maintained the balance of cells
COX2↓,
NF-kB↓,
PDK1↓, After the chrysin was injected, the genes PDK1, PDK3, and GLUT1 that are involved in glycolysis had less expression
PDK3↑,
GLUT1↓,
Glycolysis↓, chrysin stops glycolysis
mt-ATP↓, chrysin inhibits complex II and ATPases in the mitochondria of cancer cells
Ki-67↓, the amounts of Ki-67, which is a sign of growth, and c-Myc in the tumor tissues went down
cMyc↓,
ROCK1↓, (ROCK1), transgelin 2 (TAGLN2), and FCH and Mu domain containing endocytic adaptor 2 (FCHO2) were much lower.
TOP1↓, DNA topoisomerases and histone deacetylase were inhibited, along with the synthesis of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and (IL-1 beta), while the activity of protective signaling pathways was increased
TNF-α↓,
IL1β↓,
CycB/CCNB1↓, Chrysin suppressed cyclin B1 and CDK2 production in order to stop cancerous growth.
CDK2↓,
EMT↓, chrysin treatment can also stop EMT
STAT3↓, chrysin block the STAT3 and NF-B pathways, but it also greatly reduced PD-L1 production both in vivo and in vitro.
PD-L1↓,
IL2↑, chrysin increases both the rate of T cell growth and the amount of IL-2
BioAv↓, Despite its therapeutic promise, clinical application is constrained by rapid metabolism, poor bioavailability, and inconsistent biodistribution.
NF-kB↓, EGCG modulates oncogenic pathways via NF-κB suppression, caspase activation, and MMP-9 downregulation, demonstrating efficacy across diverse cancer types.
Casp↑,
MMP9↑,
Sp1/3/4↑, marked decrease in Sp1 activity
AntiCan↑, garnered significant interest for its anti-cancer effects
TumCP↓, activities against cancer, affecting various aspects of cancer cell biology, such as proliferation, cell cycle, apoptosis, metastasis, angiogenesis, and signaling pathways, such as NF-κB (Nuclear factor-KappaB), MAPK (Mitogen-activated protein kinase
TumCCA↑,
TumMeta↓,
angioG↓,
NF-kB↓,
MAPK↓,
PI3K↓,
Akt↓,
mTOR↓,
BioAv↓, its low bioavailability and solubility limit its potential clinical application.
*antiOx↑, including anti-oxidant [35], anti-inflammatory, anti-bacterial [36], anti-thrombotic or anti-platelet [37], anti-stress [38], anti-anxiety, anti-Alzheimer [39], Alzheimer, anti-stroke
*Inflam↓,
*AntiAg↑,
ChemoSen↑, administration of MG enhanced the effect of cisplatin in reducing cell viability, self-renewal, and invasion activities in cancer stem cells
cycD1/CCND1↓, Downregulation of Cyclin D1/E/B1, CDK2/4
CycB/CCNB1↓,
cycE/CCNE↓,
CDK2↓,
CDK4↓,
p27↑, upregulation of p27
P21↑, Upregulation of p21, p53
P53↑,
PTEN↓, Inhibition of PTEN
XIAP↓, Downregulation of XIAP, c-P, and Mc1-1
Mcl-1↓,
Casp3↑, upregulation of Caspase-3/9 NF-κB activity, p-p65, p-MMP-9, and cyclin
Casp9↑,
MMP9↑, Inhibiting MMP-9 through the NF-κB pathway
*eff↓, evidence suggests that frequencies higher than 100 Hz, flux densities between 1 and 10 mT, and chronic exposure more than 10 days would be more effective in establishing a cellular response
eff↝, undifferentiated PC12 cells are more sensitive to PEMF exposure, while differentiated PC12 cells are more resistant to stress
*Hif1a↑, Retinal pigment epithelial (RPE) cells Frequency of 50 Hz Intensity of 1 mT : HIF-1α, VEGFA, VEGFR-2, CTGF, cathepsin D TIMP-1, E2F3, MMP-2, and MMP-9) increased
*VEGF↑,
*TIMP1↑,
*E2Fs↑,
*MMP2↑,
*MMP9↑,
Apoptosis↑, MCF7, MCF10 Frequencies of 20 and 50 Hz Intensities of 2.0, 3.0, and 5.0 mT Cell apoptosis
MMP2↑, The 4 h LMF exposure caused a significant increase in MMP2 and MMP9, as well as in onco-miRs miR-155, miR-210, miR-21
MMP9↑,
miR-21↑,
miR-155↑, 57x
miR-210↑,
miR-200c↓, 1.25 fold decrease
miR-126↓, 2.5-fold decrease
*COX2↓, ELF‐EMF exposure enhances the proliferation of keratinocyte HaCaT cells and improves early NOS activity, while decreases cyclooxygenase 2 (COX‐2) which indicates its role in accelerating the transition from inflammation phase to remodelling phase.
*Inflam↓,
*MMP9↑, Exposure to ELF‐EMF with frequency of 50 Hz and intensity of 1 mT increases cytokine release and activates the expression of MMP‐9 in human immortalized keratinocytes
*GPx↑, On the contrary, ELF‐EMF activates glutathione peroxidase with decrease in malondialdehyde in the live tissue of rats during wound healing process
*Diff↑, ELF‐EMF promotes the proliferation and differentiation of transplanted epidermal stem cells in the full‐thickness defect nude mice
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in-vitro, |
AD, |
HT22 |
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in-vivo, |
NA, |
NA |
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*Aβ↓, It was found that rosemary could reversed Aβ25–35 induced damage to mouse hippocampal neuron HT22 cells,
*Apoptosis↓, significantly improved the viability of damaged cells, and reduced apoptosis
*antiOx↑, main antioxidant compound in rosemary, carnosic acid, also has neuroprotective effects.
*neuroP↑,
*eff↑, main active carnosic acid, carnosol, rosmarinol, rosmadial, genkwanin, cirsimaritin, rosmarinic acid and caffeic acid in Rosmarinus officinalis L,
*IGF-1↑, rosemary could elevated expression of IGF1, MMP9 and decreased mRNA levels of SRC, MAPK14, compared with the control group.
*MMP9↑,
*Src↓,
*MAPK↓,
*MMP↑, Rosemary reduced Aβ-induced HT22 cell damage in AD models to enhance the mitochondrial membrane potential levels
*antiOx↑, esame oil has been shown to have antioxidant and health-promoting benefits due to its high concentration of tocopherol, phytosterol, lignan, and other components
*LDL↓, sesame oil can reduce levels of low-density lipoprotein (LDL) and decrease the risk of atherosclerosis and cardiovascular diseases.
*Aβ↓, Alzheimer’s disease is linked to the deposition of toxic cellular amyloid proteins, and the prolonged consumption of sesamol may efficiently hinder this buildup
*TNF-α↓, Figure 2
*SOD↑,
*SIRT1↑,
*Catalase↑,
*GSH↑,
*MDA↓,
*GSTs↑,
*IL4↑,
*GPx↑,
*COX2↓,
*PGE2↓,
*NO↓,
CDK2↑,
COX2↑,
MMP9↑,
ICAM-1↓,
*BDNF↑, sesame oil increased brain-derived neurotrophic factor (BDNF) and peroxisome proliferator-activated receptor gamma (PPAR-γ) levels.
*PPARγ↑,
*AChE↓, figure 2
*Inflam↓, potent antioxidant properties, which may contribute to its anti-inflammatory effects.
*HO-1↑, activation of HO-1, leading to the inhibition of the IKKα/NFκB pathway, recognized for its involvement in inflammatory processes
*NF-kB↓,
*ROS↓, sesamin was found to decrease oxidative stress markers, including malondialdehyde (MDA) and reactive oxygen species (ROS), and increase the activity of antioxidant enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px).
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in-vitro, |
Nor, |
HUVECs |
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in-vitro, |
NA, |
NA |
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*NF-kB↓, TQ improves perforator flap survival by inhibiting the NF-κB/NLRP3 pathway and promoting angiogenesis.
*NLRP3↓,
*angioG↑,
*MMP9↑, TQ treatment increased the levels of Cadherin-5, MMP9, and VEGF
*VEGF↑,
*OS↑, TQ enhances the survival rate and angiogenesis of multi-regional perforator flaps.
*Pyro?, TQ inhibits pyroptosis after ischemia-reperfusion injury in rat perforator flaps
*ROS↓, TQ ameliorates oxidative stress and apoptosis following ischemia-reperfusion injury in rat perforator flaps
*Apoptosis↓,
*SIRT1↑, Western blot analysis revealed that SIRT1 protein expression increased after TQ treatment,
*SOD1↑, TQ treatment increased the protein expression levels of SOD1, HO1, and eNOS in rat perforator flap tissues, t
*HO-1↑,
*eNOS↑,
*ASC?, In our current experiments, we found that TQ reduced the expression of NLRP3, GSDMD-N, Caspase-1, IL-1β, IL-18, and ASC proteins both in vivo and in vitro.
*Casp1↓,
*IL1β↓,
*IL18↓,
Showing Research Papers: 1 to 11 of 11
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
lipid-P↑, 1, NRF2↓, 1, ROS↓, 1, ROS↑, 5,
Mitochondria & Bioenergetics ⓘ
mt-ATP↓, 1, MMP↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
cMyc↓, 1, Glycolysis↓, 1, PDK1↓, 1, PDK3↑, 1,
Cell Death ⓘ
Akt↓, 2, Apoptosis↑, 2, Casp↑, 2, Casp3↑, 1, Casp9↑, 1, Cyt‑c↑, 1, MAPK↓, 1, Mcl-1↓, 1, p27↑, 1,
Kinase & Signal Transduction ⓘ
Sp1/3/4↑, 1,
Transcription & Epigenetics ⓘ
miR-21↑, 1,
Protein Folding & ER Stress ⓘ
ER Stress↑, 2,
DNA Damage & Repair ⓘ
P53↑, 1, PCNA↓, 1,
Cell Cycle & Senescence ⓘ
CDK2↓, 2, CDK2↑, 1, CDK4↓, 1, CycB/CCNB1↓, 2, cycD1/CCND1↓, 1, cycE/CCNE↓, 1, P21↑, 1, TumCCA↑, 2,
Proliferation, Differentiation & Cell State ⓘ
EMT↓, 1, EMT↑, 1, mTOR↓, 2, NOTCH1↑, 1, PI3K↓, 2, PTEN↓, 1, STAT3↓, 1, STAT3↑, 1, TOP1↓, 1,
Migration ⓘ
p‑FAK↓, 1, Ki-67↓, 1, miR-155↑, 1, miR-200c↓, 1, MMP2↓, 1, MMP2↑, 1, MMP9↑, 7, Rho↓, 1, ROCK1↓, 1, TumCI↑, 1, TumCMig↑, 1, TumCP↓, 2, TumMeta↓, 2, TumMeta↑, 1, uPA↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EPR↝, 1, Hif1a↑, 1, miR-126↓, 1, miR-210↑, 1, VEGF↓, 1,
Barriers & Transport ⓘ
BBB↑, 2, GLUT1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, COX2↑, 1, ICAM-1↓, 1, IL1↑, 1, IL1β↓, 1, IL2↑, 1, IL8↑, 1, NF-kB↓, 3, PD-L1↓, 1, TNF-α↓, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 3, BioAv↑, 1, ChemoSen↑, 1, eff↑, 3, eff↝, 1, Half-Life↓, 1, RadioS↑, 1,
Clinical Biomarkers ⓘ
AR↓, 1, GutMicro↝, 1, Ki-67↓, 1, PD-L1↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1,
Total Targets: 88
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 3, Catalase↑, 2, GPx↑, 3, GSH↑, 1, GSTs↑, 1, HO-1↑, 2, MDA↓, 2, ROS↓, 3, SOD↑, 2, SOD1↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
LDL↓, 1, PPARγ↑, 1, SIRT1↑, 2,
Cell Death ⓘ
Apoptosis↓, 2, Casp1↓, 1, MAPK↓, 1, Pyro?, 1,
Cell Cycle & Senescence ⓘ
E2Fs↑, 1,
Proliferation, Differentiation & Cell State ⓘ
Diff↑, 1, IGF-1↑, 1, Src↓, 1,
Migration ⓘ
AntiAg↑, 1, MMP2↑, 1, MMP9↑, 4, TIMP1↑, 1,
Angiogenesis & Vasculature ⓘ
angioG↑, 1, eNOS↑, 1, Hif1a↑, 1, NO↓, 1, VEGF↑, 2,
Immune & Inflammatory Signaling ⓘ
ASC?, 1, COX2↓, 2, IL18↓, 1, IL1β↓, 1, IL4↑, 1, Inflam↓, 4, NF-kB↓, 2, PGE2↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, BDNF↑, 1,
Protein Aggregation ⓘ
Aβ↓, 2, NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
eff↓, 1, eff↑, 1,
Functional Outcomes ⓘ
hepatoP↑, 1, neuroP↑, 2, OS↑, 1,
Total Targets: 49
Scientific Paper Hit Count for: MMP9, MMP9
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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