TIMP2 Cancer Research Results

TIMP2, Tissue Inhibitor of Metalloproteinases-2: Click to Expand ⟱
Source:
Type:
TIMP-2 has been shown to have distinct effects on cancer progression compared to TIMP-1. Research has suggested that TIMP-2 may have anti-tumor effects in certain types of cancer, including:
• Inhibiting tumor growth: TIMP-2 has been shown to inhibit the growth of tumor cells in vitro and in vivo.
High levels of TIMP-2 have been associated with better prognosis and improved survival in some cancers.
High levels of TIMP-2 have been associated with better prognosis and improved survival in some cancers.
High TIMP-2 expression: Breast, Lung, colorectal, Prostrate.
Low TIMP-2 expression: Ovarian, Pancreatic, Gastric.
Scientific Papers found: Click to Expand⟱
2606- Ba,    Baicalein: A review of its anti-cancer effects and mechanisms in Hepatocellular Carcinoma
- Review, HCC, NA
ChemoSen↑, In addition, the combination of baicalein and silymarin eradicates HepG2 cells efficiently superior to baicalein or silymarin alone
TumCP↓, Cell viability assays have demonstrated that baicalein is significantly cytotoxic against several HCC cell lines and can inhibit the proliferation of HCC cells through arresting the cell cycle.
TumCCA↑,
TumCMig↓, Baicalein has been proved to inhibit migration and invasion of human HCC cells by reducing the expression and their proteinase activity of matrix metalloproteinases (MMPs),
TumCI↓,
MMPs↓,
MAPK↓, A large number of studies found that baicalein could inhibit migration and invasion of cancer cells by targeting the MAPK, TGF-b/Smad4, GPR30 pathway and molecules such as, ezrin, zinc-finger protein X-linked (ZFX),
TGF-β↓,
ZFX↓,
p‑MEK↓, Baicalein could inhibited the phosphorylation of MEK1 and ERK1/2, leading to decreased expression and proteinase activity of MMP-2/9 and urokinase-type plasminogen activator (u-PA),
ERK↓,
MMP2↓,
MMP9↓,
uPA↓,
TIMP1↓, as well as increased expression of TIMP-1 and TIMP-2
TIMP2↓,
NF-kB↓, Additionally, the nuclear translocation of NF-kB/p50 and p65/RelA and the phosphorylation of I-kappa-B (IKB)-b could be down-regulated by baicalein
p65↓,
p‑IKKα↓,
Fas↑, Hep3 B cells via activating Fas, Caspase -2, -3, -8, -9, down-regulating Bcl-xL, and upregulating Bax [
Casp2↑,
Casp3↑,
Casp8↑,
Casp9↑,
Bcl-xL↓,
BAX↑,
ER Stress↑, baicalein could induced apoptosis via endoplasmic reticulum (ER) stress in SMMC-7721 and Bel-7402
Ca+2↑, increasing intracellular calcium(Ca2+ ), and activating JNK pathwa
JNK↑,
P53↑, selectively induce apoptosis in HCC J5 cells via upregulation of p53
ROS↑, baicalein could induced cell apoptosis through regulating ROS via increasing intracellular H2O 2 level [
H2O2↑,
cMyc↓, baicalein could promote apoptosis in HepG2 and Bel-7402 cells through inhibiting c-Myc and CD24 expression
CD24↓,
12LOX↓, baicalein could induced cell apoptosis in SMMC-7721 and HepG2 cells by specifically inhibiting expression of 12-lipoxygenase(12-LOX), a critical anti-apoptotic genes

2617- Ba,    Potential of baicalein in the prevention and treatment of cancer: A scientometric analyses based review
- Review, Var, NA
Ca+2↑, MDA-MB-231 ↑Ca2+
MMP2↓, MDA-MB-231 ↓MMP-2/9
MMP9↓,
Vim↓, ↓Vimentin, ↓SNAIL, ↑E-cadherin, ↓Wnt1, ↓β-catenin
Snail↓,
E-cadherin↑,
Wnt↓,
β-catenin/ZEB1↓,
p‑Akt↓, MCF-7 ↓p-Akt, ↓p-mTOR, ↓NF-κB
p‑mTOR↓,
NF-kB↓,
i-ROS↑, MCF-7 ↑Intracellular ROS, ↓Bcl-2, ↑Bax, ↑cytochrome c, ↑caspase-3/9
Bcl-2↓,
BAX↑,
Cyt‑c↑,
Casp3↑,
Casp9↑,
STAT3↓, 4T1, MDA-MB-231 ↓STAT3, ↓ IL-6
IL6↓,
MMP2↓, HeLa ↓MMP-2, ↓MMP-9
MMP9↓,
NOTCH↓, ↓Notch 1
PPARγ↓, ↓PPARγ
p‑NRF2↓, HCT-116 ↓p-Nrf2
HK2↓, ↓HK2, ↓LDH-A, ↓PDK1, ↓glycolysis, PTEN/Akt/HIF-1α regulation
LDHA↓,
PDK1 / PDPK1↓,
Glycolysis↓,
PTEN↑, Furthermore, baicalein inhibited hypoxia-induced Akt phosphorylation by promoting PTEN accumulation, thereby attenuating hypoxia-inducible factor-alpha ( HIF-1a) expression in AGS cells.
Akt↓,
Hif1a↓,
MMP↓, SGC-7901 ↓ΔΨm
VEGF↓, ↓VEGF, ↓VEGFR2
VEGFR2/KDR/Flk1↓,
TOP2↓, ↓Topoisomerase II
uPA↓, ↓u-PA, ↓TIMP1, ↓TIMP2
TIMP1↓,
TIMP2↓,
cMyc↓, ↓β-catenin, ↓c-Myc, ↓cyclin D1, ↓Axin-2
TrxR↓, EL4 ↓Thioredoxin reductase, ↑ASK1,
ASK1↑,
Vim↓, ↓vimentin
ZO-1↑, ↑ZO-1
E-cadherin↑, ↑E-cadherin
SOX2↓, PANC-1, BxPC-3, SW1990 ↓Sox-2, ↓Oct-4, ↓SHH, ↓SMO, ↓Gli-2
OCT4↓,
Shh↓,
Smo↓,
Gli1↓,
N-cadherin↓, ↓N-cadherin
XIAP↓, ↓XIAP

7567- HYP,    Hyperoside: A review on its sources, biological activities, and molecular mechanisms
- Review, Var, NA
*AntiCan↑, anticancer, anti-inflammatory, antibacterial, antiviral, antidepressant, and organ protective effects.
*Bacteria↓,
*AntiViral↑,
*antiD↓,
*RenoP↑, Kidney protection
*hepatoP↑, Liver protection
*eff↑, treating multiple diseases, such as sepsis, arthritis, colitis, diabetic nephropathy, myocardial ischemia-reperfusion, pulmonary fibrosis, and cancers.
*Sepsis↓,
*AntiArt↑,
*Stroke↓,
TumCMig↓, hyperoside has been shown to inhibit the migration and invasion properties of A549 cells by suppressing the expression of metastasis-associated gene 1 (MTA1), matrix metalloproteinase-2 inhibitor (TIMP-2), matrix metalloproteinase (MMP)-2
TumCI↓,
MTA1↓,
TIMP2↓,
MMP2↓,
MMP↓, disrupted the penetration of the mitochondrial membrane, and triggered mitochondrial cytochrome C and apoptosis inducers into the cytoplasm
Cyt‑c↑,
Akt↓, inhibited the Akt/mTOR/p70S6K signaling pathway in NSCLC cells to promote autophagy and exerted anticancer activity
mTOR↓,
P70S6K↓,
TumAuto↑,
PD-L1↓, thereby inhibiting PD-L1 expression at the transcriptional leve
TNF-α↓, subsequently, inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1b, IL-6 and IL-8, were significantly down-regulated
IL1β↓,
IL6↓,
IL8↓,
Bcl-2↓, Hyperoside was reported to inhibit the over-expression of B-cell lymphoma factor 2 (Bcl)-2 and Bcl-x in lung cancer cells, and up-regulate the preapoptotic factors such as Bax, Bad, and Bak.
Bcl-xL↓,
BAX↑,
BAD↑,
Bak↑,
VEGF↓, decreasing the HeLa cell's vascular endothelial growth factor (VEGF) expression levels in HeLa cells.
Casp3↑, hyperoside promoted apoptosis via enhancing caspase-3 and caspase-8 protein expression, and on the other hand, by promoting tumor suppressor gene P35 expression
Casp8↑,
P53↑,
GSH↓, Hyperoside could also reduce glutathione levels in HeLa cells, superoxide dismutase (SOD), and Catalase (CAT) viability.
SOD↓,
Catalase↓,
TAC↓, reduced the antioxidant capacity and thus to inhibit cancer cell growth
XIAP↓, MCF-7 and 4 T1 cells Decreased the levels of Bcl-2 and XIAP; increased the levels of Bax and cleaved cysteine protease-3; decreased the production of ROS and inhibited NFκB signal pathway
ROS↓,
NF-kB↓,
TLR4↓, MDA-MB-231 cells Inhibited TLR4-NF-κB signaling pathways; decreased the expression of Bcl-2; enhanced the expression of pro-apoptotic Bax and the level of pro-inflammatory cytokine IL-6
P-gp/ABCB1↓, S180 cancer cell Reduced the expression of P-gp, LRP and Bcl-2 and increased the expression of Fas; inhibited bad phosphorylation and increased p27 level
LRP1↓,
Fas↑,
p27/CDKN1B↑,
*cardioP↑, Cardiovascular protection In vivo pulmonary embolism and arterial thrombosis model Prolonged the activated prothrombin time and suppressed thrombin and FXa activities; inhibit the production of PAI-1 induced by TNF-α
*AntiThr↑,
*PAI-1/SERPINE1↓,
*BUN↓, Reduced the contents of serum angiotensin converting enzyme ArgII, ALD, U-mAlb, BUN, SCR, ALT, and AST
*ALAT↓,
*AST↓,
*neuroP?, Neuroprotection

7695- IP6,    The effect of inositol hexaphosphate on the expression of selected metalloproteinases and their tissue inhibitors in IL-1β-stimulated colon cancer cells
- in-vitro, Colon, Caco-2
AntiCan↑, Inositol hexaphosphate (IP6 phytic acid) has been recognized to have both preventive and therapeutic effects against various cancers including that of colon.
TumCA↓, IP6 has been demonstrated to inhibit cancer cell adhesion and migration.
TumCMig↓,
MMP13↓, A significant decrease in MMP-13, MMP-3, MMP-2, and TIMP-1 basal expression was achieved by IP6.
MMP3↓,
MMP2↓,
TIMP1↓,
MMP1↓, IP6 was also an efficient downregulator of MMP-1, MMP-9, and TIMP-2 genes transcription stimulated by IL-1β in 6 h lasting culture.
MMP9↓,
TIMP2↓,

8105- KAE,    Chemo-preventive and therapeutic effect of the dietary flavonoid kaempferol: A comprehensive review
- Review, Var, NA
Apoptosis↑, It induces apoptosis (HeLa cervical cancer cells), decreases cell viability (G2/M phase), downregulates phosphoinositide 3-kinase (PI3K)/AKT
tumCV↓,
TumCCA↑,
PI3K↓,
Akt↓,
EMT↓, suppresses protein expression of epithelial-mesenchymal transition (EMT)-related markers including N-cadherin, E-cadherin, Slug, and Snail, and metastasis-related markers such as matrix metallopeptidase 2 (MMP-2).
N-cadherin↓,
E-cadherin↓, nhibition of N‐cadherin, E‐cadherin, Slug, Snail, and MMP‐2, 9, and cathepsin B, D
Slug?,
Snail?,
MMP2↓,
MMP9↓,
CTSB↓,
CTSD↓,
Casp3↑, Activation of caspase signals such as caspase‐3, ‐8, and ‐9
Casp8↑,
Casp9↑,
TIMP2↓, Down‐regulation of phosphorylated TIMP2, AKT, and MMP2 levels
Akt↓,
TumCD↑, Induction of cell apoptotic cell death, intracellular free calcium elevation, and mitochondrial membrane potential disruption.
i-Ca+2↑,
MMP↓,
*ROS↓, Enhances the concentrations of superoxide dismutase, catalase, glutathione peroxidase, and glutathione‐S‐transferase.
*SOD↑,
*Catalase↑,
*GPx↑,
*GSTs↑,
*AST↓, Lowers aspartate aminotransferase, alanine aminotransferase, malondialdehyde (MDA).
*ALAT↓,
*MDA↓,
*CYP2E1↓, Decreases activity of hepatic microsomal enzyme cytochrome 2E1 (CYP2E1) expression
*NRF2↑, Increases mRNA and protein expression of Nrf2‐regulated genes
*AGEs↓, Suppresses advanced glycation end products (AGEs)‐ receptor.
*IL6↓, Reduces levels of IL‐6, TNF‐α, and NF‐κB.
*TNF-α↓,
*NF-kB↓,
*Casp3↓, Lowers expressions of Caspase‐3 and Bax,
*BAX↓,
*antiAll↑, Antiallergic Inhibits COX2‐mediated production of prostaglandin D2 and prostaglandin F2α.
*COX2/PTGS2↓,
*PGE2↓,
*RUNX2↑, Increases expression of the osteoblast‐activated factors RUNX‐2, BMP‐2, osterix, collagen I, and SQSTM1/p62
*BMP2↑,
*COL1↑,
*p62↑,
*FASN↓, Reduces expressions of lipin1, FASN, LPAATθ (lysophosphatidic acid acyltransferase), SREBP‐1C (fatty acid synthetic proteins), and DGAT1 (triglyceride synthetic enzymes).
*DGAT1↓,
FOXP3↑, kaempferol significantly enhanced the inhibitory effect of proliferation, increased the FOXP3 expression level,
DNAdam↑, s induction of DNA damage, enhancement DNA condensation
ROS↑, anti‐cancer property is mainly defined by ROS accumulation due to catalase inhibition as depicted in Figure 2
Catalase↓,
*ROS↓, (A/R)‐induced injury of cardiomyocytes by increasing cell viability, lowering LDH release, reducing A/R‐induced ROS generation, loss of Δψm, and release of cytochrome c from mitochondria into cytosol.
*MMP↑,
*Cyt‑c↓,

8055- KAE,    Molecular Mechanisms of the Anticancer Activity of the Flavonoid Kaempferol: A Comprehensive Review
- Review, Var, NA
antiNeop↑, Kaempferol (KAE), a natural flavonoid, has emerged as a promising multi-target antineoplastic agent characterized by high efficacy and minimal systemic toxicity.
*toxicity↓,
TumCCA↑, KAE orchestrates tumor eradication by enforcing cell cycle arrest across multiple phases and triggering a complex, interconnected network of programmed cell death.
ROS↑, We highlight how reactive oxygen species and endoplasmic reticulum stress serve as central upstream nodes driving the mechanistic crosstalk among apoptosis, lethal autophagy, gasdermin E-mediated pyroptosis, and ferroptosis.
ER Stress↑,
TumAuto↑,
Pyro↑,
Ferroptosis↑,
angioG↓, KAE actively remodels the tumor microenvironment by inhibiting angiogenesis and repolarizing tumor-associated macrophages, thereby converting immunosuppressive "cold" tumors into immune-active "hot" tumors.
Imm↝,
eff↑, this review introduces the emerging prebiotic-like crosstalk between KAE and the gut microbiome, providing a strong mechanistic rationale for its synergistic application with immune checkpoint inhibitors.
ChemoSen↑, As a potent chemosensitizer, KAE also overcomes multidrug resistance and mitigates chemotherapy-induced toxicities.
MPT↑, This leads to the opening of the mitochondrial permeability transition (MPTP) pore and the collapse of the mitochondrial membrane potential (ΔΨm).
MMP↓,
mtDam↑, damaged mitochondria release pro-apoptotic factors, including cytochrome c, into the cytoplasm, inducing the formation of the apoptosome.
Cyt‑c↑,
Bax:Bcl2↑, upregulation of the Bax/Bcl-2 ratio.
Fas↑, demonstrated that in colorectal cancer models, KAE treatment significantly upregulates the expression of membrane-bound FAS ligand.
DR4↑, KAE directly upregulates the expression of death receptor 4 and death receptor 5 in human ovarian cancer cells (OVCAR-3 and SKOV-3) by activating the JNK/ERK-CHOP signaling pathway.
DR5↑,
JNK↑,
ERK↑,
CHOP/DDIT3↑,
ER Stress↑, Studies have shown that KAE possesses significant ERS-inducing activity, leading to the pathological accumulation of unfolded or misfolded proteins within the endoplasmic reticulum (ER) lumen, which in turn triggers a persistent unfolded protein resp
UPR↑,
Ca+2↑, accumulated cytosolic Ca²+ acts as a central apoptotic signal
PI3K↓, The inhibition of the PI3K/Akt/mTOR pathway is a primary mechanism for this effect.
Akt↓,
mTOR↓,
AMPK↑, Conversely, KAE reactivates the AMPK pathway.
*Ferroptosis↓, KAE acts as a potent antioxidant in normal tissues to prevent ferroptosis-induced injury.
*antiOx↑,
*NRF2↑, KAE effectively suppresses ferroptosis by strongly activating the Nrf2/glutathione peroxidase 4 (GPX4) antioxidant axis.
*GPx4↑,
*ROS↓, It actively reduces intracellular ROS, malondialdehyde, and iron (Fe²+) accumulation while upregulating the protective SLC7A11 transporter
*MDA↓,
*i-Iron↓,
*xCT/SLC7A11↑,
VEGF↓, KAE not only inhibits VEGF expression driven by hypoxia-inducible factor-1α (HIF-1α) but also simultaneously blocks the Wnt/β-catenin signaling pathway and the epithelial-mesenchymal transition (EMT) process
Wnt↓,
β-catenin/ZEB1↓,
EMT↓,
STAT3↓, KAE blocks the persistent activation of the STAT3 signaling pathway, leading to the downregulation of M2 phenotypic markers and the inhibition of the inflammatory chemokine CCL2 release.
M2 MC↓,
MCP1/CCL2↓,
MMP9↓, thereby downregulating the protein expression and enzymatic activity of MMP-9.
MMP2↓, in tongue squamous cell carcinoma models, KAE inhibits the expression of MMP-2 and its tissue inhibitor, TIMP-2, at the transcriptional level
TIMP2↓,
ChemoSen↑, When combined with classical chemotherapeutics, KAE functions as a potent sensitizer, amplifying the lethal effects of the drugs through complementary signaling networks.
PKM2↑, In colorectal cancer cells, KAE promotes the expression of microRNA-326 (miR-326), which directly targets the 3′-UTR of the pyruvate kinase M2 (PKM2) isoform to inhibit glycolysis.
Glycolysis↓,
CSCs↓, profound chemosensitizing effect by downregulating core stemness transcription factors (such as SOX2 and OCT4) and disrupting the CD44-NANOG-MDR1 resistance complex
SOX4↓,
OCT4↓,
CD44↓,
Nanog↓,
MDR1↓,
*GutMicro↑, KAE exerts a remarkable prebiotic-like effect by remodeling the architectural composition of the gut microbiota


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned(tgid=0) ⓘ

MTA1↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↓, 2,   Ferroptosis↑, 1,   GSH↓, 1,   H2O2↑, 1,   p‑NRF2↓, 1,   ROS↓, 1,   ROS↑, 3,   i-ROS↑, 1,   SOD↓, 1,   TAC↓, 1,   TrxR↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

p‑MEK↓, 1,   MMP↓, 4,   MPT↑, 1,   mtDam↑, 1,   XIAP↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

12LOX↓, 1,   AMPK↑, 1,   cMyc↓, 2,   Glycolysis↓, 2,   HK2↓, 1,   LDHA↓, 1,   PDK1 / PDPK1↓, 1,   PKM2↑, 1,   PPARγ↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 5,   p‑Akt↓, 1,   Apoptosis↑, 1,   ASK1↑, 1,   BAD↑, 1,   Bak↑, 1,   BAX↑, 3,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Bcl-xL↓, 2,   Casp2↑, 1,   Casp3↑, 4,   Casp8↑, 3,   Casp9↑, 3,   Cyt‑c↑, 3,   DR4↑, 1,   DR5↑, 1,   Fas↑, 3,   Ferroptosis↑, 1,   JNK↑, 2,   MAPK↓, 1,   p27/CDKN1B↑, 1,   Pyro↑, 1,   TumCD↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↑, 1,   ER Stress↑, 3,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

TumAuto↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   P53↑, 2,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 3,  

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

CD24↓, 1,   CD44↓, 1,   CSCs↓, 1,   CTSB↓, 1,   CTSD↓, 1,   EMT↓, 2,   ERK↓, 1,   ERK↑, 1,   Gli1↓, 1,   mTOR↓, 2,   p‑mTOR↓, 1,   Nanog↓, 1,   NOTCH↓, 1,   OCT4↓, 2,   P70S6K↓, 1,   PI3K↓, 2,   PTEN↑, 1,   Shh↓, 1,   Smo↓, 1,   SOX2↓, 1,   STAT3↓, 2,   TOP2↓, 1,   Wnt↓, 2,   ZFX↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 3,   i-Ca+2↑, 1,   E-cadherin↓, 1,   E-cadherin↑, 2,   LRP1↓, 1,   MMP1↓, 1,   MMP13↓, 1,   MMP2↓, 7,   MMP3↓, 1,   MMP9↓, 6,   MMPs↓, 1,   N-cadherin↓, 2,   Slug?, 1,   Snail?, 1,   Snail↓, 1,   SOX4↓, 1,   TGF-β↓, 1,   TIMP1↓, 3,   TIMP2↓, 6,   TumCA↓, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 1,   uPA↓, 2,   Vim↓, 2,   ZO-1↑, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   VEGF↓, 3,   VEGFR2/KDR/Flk1↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

FOXP3↑, 1,   p‑IKKα↓, 1,   IL1β↓, 1,   IL6↓, 2,   IL8↓, 1,   Imm↝, 1,   M2 MC↓, 1,   MCP1/CCL2↓, 1,   NF-kB↓, 3,   p65↓, 1,   PD-L1↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 3,   eff↑, 1,   MDR1↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 2,   PD-L1↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   antiNeop↑, 1,  
Total Targets: 134

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

antiAll↑, 1,   AntiArt↑, 1,   antiD↓, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   CYP2E1↓, 1,   Ferroptosis↓, 1,   GPx↑, 1,   GPx4↑, 1,   GSTs↑, 1,   i-Iron↓, 1,   MDA↓, 2,   NRF2↑, 2,   ROS↓, 3,   SOD↑, 1,   xCT/SLC7A11↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 2,   BUN↓, 1,   DGAT1↓, 1,   FASN↓, 1,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   BMP2↑, 1,   Casp3↓, 1,   Cyt‑c↓, 1,   Ferroptosis↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

p62↑, 1,  

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

RUNX2↑, 1,  

Migration(tgid=13) ⓘ

COL1↑, 1,   PAI-1/SERPINE1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL6↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

AGEs↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 2,   AST↓, 2,   GutMicro↑, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   cardioP↑, 1,   hepatoP↑, 1,   neuroP?, 1,   RenoP↑, 1,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiViral↑, 1,   Bacteria↓, 1,   Sepsis↓, 1,  
Total Targets: 52

Scientific Paper Hit Count for: TIMP2, Tissue Inhibitor of Metalloproteinases-2
2 Baicalein
2 Kaempferol
1 Hyperoside
1 IP6 (Inositol 1,2,3,4,5,6-hexakisphosphate)
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#:308  State#:%  Dir#:1
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