SMAD3 Cancer Research Results

SMAD3, SMAD3: Click to Expand ⟱
Source:
Type:
Deletion or inhibition of Smad3 in the tumour microenvironment suppresses tumour growth, invasion and metastasis in two syngeneic mouse tumour models.
Smad3 promotes cancer progression by inhibiting E4BP4-mediated NK cell development.
Scientific Papers found: Click to Expand⟱
5553- BBM,    A review on berbamine–a potential anticancer drug
- Review, Var, NA
P-gp/ABCB1↓, Treatment with berbamine decreased P-glycoprotein (P-gp) expression and down-regulated expression of MDR1 (multi-drug resistance1) and survivin mRNA in K562/A02 cells
MDR1↓,
survivin↓,
NF-kB↓, decrease expression of nuclear factor-B (NF-B), phosphoIB, IKK, and survivin.
TumCP↓, In a chronic myeloid leukemia cell line KU812, berbamine inhibited cell proliferation in a time- and dose-dependent manner, with IC50 values for treatments of 24, 48, and 72 h at 5.83, 3.43, and 0.75 μg/ml, respectively.
TumCCA↑, Berbamine induced cell cycle arrest at the G1 phase and also induced apoptosis.
Apoptosis↑,
SMAD3↑, The compound up-regulated transcriptions of Smad3 and p21, and increased protein levels of both total Smad3 and phosphorylated Smad3.
P21↑,
cycD1/CCND1↓, The protein levels of cyclin D1 and c-Myc were reduced.
cMyc↑,
Bcl-2↓, The levels of the anti-apoptotic proteins Bcl-2 and Bcl-xL were decreased, and the level of the pro-apoptotic protein Bax was increased.
Bcl-xL↓,
BAX↑,
CaMKII ↓, The compound has been shown to specifically bind to the ATP-binding pocket of calmodulin kinase (CAMK)II, inhibit its phosphorylation, and trigger apoptosis.
ChemoSen↑, Berbamine also significantly enhanced the activity of anticancer drugs like trichostatin A and celecoxib.
MMP2↓, EBB down-regulated the activities and mRNA levels of matrix metalloproteinases (MMP) 2 and 9, and up-regulated the mRNA levels of tissue inhibitor of metalloproteinases (TIMP) 1.
MMP9↓,
TIMP1↑,
cl‑Casp3↑, induction of apoptosis, including activation and cleavage of caspases 3, 8, 9 and PARP.
cl‑Casp9↑,
cl‑Casp8↑,
cl‑PARP↑,
IL6↓, BBD inhibited autocrine IL-6 production, and down-regulated membrane IL-6 receptor (IL-6R) expression.
ROS↑, Production of reactive oxygen species (ROS) was increased by BBMD3 in these cells.

8080- KAE,    Hepatoprotective Effect of Kaempferol—A Review
- Review, Nor, NA
*hepatoP↑, Kaempferol, a naturally occurring flavonoid, has demonstrated significant hepatoprotective effects in preclinical models
*SIRT1↑, This substance activates the SIRT1/AMPK signalling pathway, improves mitochondrial function, inhibits proinflammatory cytokine production via TLR4/NF-κB suppression and attenuates hepatic stellate cell activation by modulating the TGF-β/Smad pathwa
*AMPK↑,
*TLR4↓,
*NF-kB↓,
*GutMicro↑, kaempferol regulates the composition of the gut microbiota, thus improving bile acid metabolism and alleviating steatosis and fibrosis.
*Dose↝, The most significant amounts of kaempferol can be found in vegetables such as kale, spinach, onions, or beverages, especially black or green tea infusions
*BioAv↓, the bioavailability of the various chemical forms of oral kaempferol is low and has been calculated to be around 2%
*BioAv↑, However, there are some modern approaches (nanoparticles, structural modifications, chimeric molecules) that could certainly be exploited to improve kaempferol bioavailability [
*CYP2E1↓, including SIRT1 activation, CYP2E1 inhibition, TLR4/NF-κB suppression and ALK5/Smad pathway interference
*lipidLev↓, Reduction of Hepatic Lipid Accumulation
*COX2/PTGS2↓, Kaempferol can also suppress the production and expression of COX-2, IL-1β, TNF-α, and IL-6 mRNA, which play key roles in inflammation
*IL1β↓,
*TNF-α↓,
*IL6↓,
*NO↓, reduces the levels of NO and PGE2 while lowering iNOS mRNA expression in cases of acute liver injury.
*PGE2↓,
*iNOS↓,
*SOD↑, increased SOD activity and decreased MDA levels in the liver were observed when compared with the haemorrhagic shock group.
*MDA↓,
*ROS↓, inhibit CYP2E1 at both the expression and activity levels, consequently leading to a reduction in ROS levels and liver damage.
*AST↓, The significant decrease in serum AST and ALT levels is due to this inhibitory effect.
*ALAT↓,
*GSH↑, The induction of reactive antioxidant enzymes (GSH and SOD) by this compound
*SOD↑,
*Cyt‑c↓, inhibiting hepatocyte apoptosis through the reduction of apoptosis-related proteins, including cytochrome c, Bax, Bcl-2, caspases:3, 8 and 9
*BAX↓,
*Casp3↓,
*Casp8↓,
*Casp9↓,
*COL1↓, Kaempferol has been shown to be capable of inhibiting type I collagen expression in HSCs and reducing collagen density in liver tissue
*p‑SMAD2↓, reducing the phosphorylation of Smad2 and Smad3 by the serine/threonine kinase, attenuating α-SMA production, and inhibiting TGF-β-stimulated HSCs
*p‑SMAD3↑,
*α-SMA↓,
*TGF-β↓,
*P450↝, Kaempferol interacts with cytochrome P450 enzymes, including CYP3A4, which is key to drug metabolism.
*P-gp/ABCB1↓, It has been demonstrated that kaempferol is capable of inhibiting P-gp, which may consequently result in an enhancement of the bioavailability of drugs that are P-gp substrates.
*BioEnh↑,


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

cMyc↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   cl‑Casp3↑, 1,   cl‑Casp8↑, 1,   cl‑Casp9↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

CaMKII ↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Migration(tgid=13) ⓘ

MMP2↓, 1,   MMP9↓, 1,   SMAD3↑, 1,   TIMP1↑, 1,   TumCP↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL6↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   MDR1↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  
Total Targets: 26

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

CYP2E1↓, 1,   GSH↑, 1,   MDA↓, 1,   ROS↓, 1,   SOD↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   AMPK↑, 1,   lipidLev↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

BAX↓, 1,   Casp3↓, 1,   Casp8↓, 1,   Casp9↓, 1,   Cyt‑c↓, 1,   iNOS↓, 1,  

Migration(tgid=13) ⓘ

COL1↓, 1,   p‑SMAD2↓, 1,   p‑SMAD3↑, 1,   TGF-β↓, 1,   α-SMA↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 1,  

Barriers & Transport(tgid=15) ⓘ

P-gp/ABCB1↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,   IL1β↓, 1,   IL6↓, 1,   NF-kB↓, 1,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   BioEnh↑, 1,   Dose↝, 1,   P450↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

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

Functional Outcomes(tgid=23) ⓘ

hepatoP↑, 1,  
Total Targets: 39

Scientific Paper Hit Count for: SMAD3, SMAD3
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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