TIMP3 Cancer Research Results

TIMP3, tissue inhibitor of metalloproteinases-3: Click to Expand ⟱
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TIMP-3 has been shown to have tumor suppressor properties, as it inhibits the activity of MMPs, which are involved in tumor growth, invasion, and metastasis.
Scientific Papers found: Click to Expand⟱
5894- CAR,    Targeting Gastrointestinal Cancers with Carvacrol: Mechanistic Insights and Therapeutic Potential
- Review, Var, NA
AntiCan↑, Carvacrol has demonstrated strong anticancer properties by modulating multiple molecular pathways governing apoptosis, inflammation, angiogenesis, and metastasis.
Apoptosis↑,
Inflam↓,
angioG↓,
TumMeta↓,
selectivity↑, revealed its ability to selectively target cancer cells while sparing healthy tissue
BioAv↑, nanotechnology have further enhanced its pharmacological profile by improving solubility, stability, and tumor-targeted delivery.
ChemoSen↑, synergistic effects when used in combination with conventional chemotherapeutics.
Dose↝, 84.38% of OEO’s contents are ‘carvacrol’.
TumCP↓, limit metastasis, induce apoptosis, suppress tumor cell proliferation, and improve the effectiveness of traditional chemotherapy medications
hepatoP↑, Carvacrol shows biological activities, such as antimicrobial, antitumor, antimutagenic, antigenotoxic, anti-inflammatory, anti-angiogenic, hepatoprotective, and antihepatotoxic properties.
Casp3↑, induced apoptosis by activating caspase-3 and caspase-9 while downregulating Bcl-2 mRNA levels
Casp9↑,
Bcl-2↓,
ROS↑, carvacrol causes oxidative stress by increasing the production of reactive oxygen species (ROS) and depleting GSH levels, which results in strong lethal effects on AGS gastric cancer
GSH↓,
BAX↑, upregulating pro-apoptotic markers such as Bax, caspase-3, caspase-7, caspase-8, caspase-9, cytochrome C, Fas, Fas-associated death domain (FADD), and p53
Casp7↑,
Casp8↑,
Cyt‑c↑,
Fas↑,
FADD↑,
P53↑,
Bcl-2↓, downregulating anti-apoptotic Bcl-2.
TumMeta↓, preventing metastasis by limiting the migration and invasion of cancer cells by upregulating epithelial markers like E-Cadherin and tissue inhibitors of metalloproteinases 2 and 3 (TIMP2 and TIMP3)
TumCMig↓,
TumCI↓,
E-cadherin↑,
TIMP2↑,
TIMP3↑,
N-cadherin↓, downregulating mesenchymal markers like N-Cadherin and ZEB2
ZEB2↓,
*lipid-P↓, protects the liver from diethylnitrosamine (DEN)-induced hepatocellular carcinogenesis by reducing lipid peroxidation, restoring key liver enzymes (AST, ALT, ALP, LDH, cGT)
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑, and enhancing antioxidant defenses (SOD, CAT, GPx, GR, GSH)
*Catalase↑,
*GPx↑,
*GSR↑,
selectivity↑, while selectively inducing apoptosis in cancer cells without harming normal liver tissue
cl‑PARP↑, inhibits HepG2 cancer cell growth by activating caspase-3, promoting PARP cleavage, downregulating Bcl-2, and modulating the MAPK signaling pathway by selectively reducing ERK1/2 phosphorylation while activating p38
ERK↓,
p38↑,
OS↑, rats (aged 6–8 weeks) demonstrated that carvacrol enhances sorafenib efficacy in HCC, improving survival rates, reducing tumor progression, and mitigating sorafenib-induced cardiac and hepatic toxicity.
AFP↓, carvacrol reduces serum alpha-fetoprotein (AFP) and alpha-L-fucosidase (AFU) levels by downregulating COX-2 and oxidative stress, inhibits angiogenesis via VEGF suppression,
COX2↓,
VEGF↓,
PCNA↓, prevents tumor proliferation by downregulating proliferating cell nuclear antigen (PCNA) and Ki-67 through TNF-α suppression.
Ki-67↓,
TNF-α↓,
BioAv↓, Despite carvacrol’s promising effects in vitro and in vivo, limitations such as bioavailability and solubility challenge its therapeutic application.

639- EGCG,    Immunomodulatory Effects of Green Tea Catechins and Their Ring Fission Metabolites in a Tumor Microenvironment Perspective
- Review, NA, NA
TIMP3↑,
MMP2↓,
MMP9↓,

3359- QC,    Quercetin modifies 5′CpG promoter methylation and reactivates various tumor suppressor genes by modulating epigenetic marks in human cervical cancer cells
- in-vitro, Cerv, HeLa
DNMTs↓, When nuclear extracts were incubated with increasing doses of quercetin (25 and 50uM) they were found to inhibit the function of the DNMTs by 32% and 49% respectively, in comparison to untreated control
HDAC↓, quercetin (25 and 50 uM), they were found to inhibit the function of the HDACs by 47% and 62% in comparison to untreated control.
HMTs↓, quercetin (25 and 50 uM), were found to inhibit the function of the HMT H3K9 by 63% and 71%
DNMT3A↓, preferred binding of quercetin on DNMT3A and DNMT3B is within the substrate binding cavity and could competitively inhibit the protein
EZH2↓, Quercetin interacts with EZH2 and functions as an inhibitor
HDAC1↓, Quercetin was able to reduce the activity of class II HDACs significantly, with concomitant downregulation of HDAC1, HDAC2, HDAC6, HDAC7, and HDAC11 expression
HDAC2↓,
HDAC6↓,
HDAC11↓,
G9a↓, quercetin and this correlates well with the observed downregulation of G9A expression
TIMP3↑, Fig8: quercetin resulted in reduced promoter methylation of several TSGs (APC, CDH1, CDH13, DAPK1, FHIT, GSTP1, MGMT, MLH1, PTEN, RARB, RASSF1, SOC51, TIMP3, and VHL
PTEN↑,
SOCS1↑,

3086- RES,    Resveratrol inhibits the tumor migration and invasion by upregulating TET1 and reducing TIMP2/3 methylation in prostate carcinoma cells
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3 - in-vitro, Pca, DU145
TET1↑, Res upregulated the 5hmC and TET1 levels and downregulated the 5mC level.
TumCMig↓, Res also inhibited the migration and invasion of PCa cells
TumCI↓,
TIMP2↑, promoted the demethylation of TIMP2 and TIMP3 to upregulate their expressions, and suppressed the expressions of MMP2 and MMP9.
TIMP3↑,
MMP2↓,
MMP9↓,


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH↓, 1,   ROS↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 2,   Casp3↑, 1,   Casp7↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   FADD↑, 1,   Fas↑, 1,   p38↑, 1,  

Transcription & Epigenetics ⓘ

EZH2↓, 1,  

DNA Damage & Repair ⓘ

DNMT3A↓, 1,   DNMTs↓, 1,   G9a↓, 1,   P53↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC11↓, 1,   HDAC2↓, 1,   HDAC6↓, 1,   HMTs↓, 1,   PTEN↑, 1,  

Migration ⓘ

E-cadherin↑, 1,   Ki-67↓, 1,   MMP2↓, 2,   MMP9↓, 2,   N-cadherin↓, 1,   TET1↑, 1,   TIMP2↑, 2,   TIMP3↑, 4,   TumCI↓, 2,   TumCMig↓, 2,   TumCP↓, 1,   TumMeta↓, 2,   ZEB2↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Inflam↓, 1,   SOCS1↑, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

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

Clinical Biomarkers ⓘ

AFP↓, 1,   EZH2↓, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   hepatoP↑, 1,   OS↑, 1,  
Total Targets: 58

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GPx↑, 1,   GSR↑, 1,   lipid-P↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   LDH↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AST↓, 1,   LDH↓, 1,  
Total Targets: 11

Scientific Paper Hit Count for: TIMP3, tissue inhibitor of metalloproteinases-3
1 Carvacrol
1 EGCG (Epigallocatechin Gallate)
1 Quercetin
1 Resveratrol
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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