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⟱

1093-

And,

Andrographolide attenuates epithelial‐mesenchymal transition induced by TGF‐β1 in alveolar epithelial cells

in-vitro,

Lung,

A549

TGF-β↓,
TumCMig↓,
MMP2↓,
MMP9↓,
ECM/TCF↓,
p‑SMAD2↓,
p‑SMAD3↓,
SMAD4↓,
p‑ERK↓,
ROS↓, reduced (TGF‐β1‐induced) intracellular ROS generation
NOX4↓,
SOD2↑,
SIRT1↑, Andro protects AECs from EMT partially by activating Sirt1/FOXO3‐mediated anti‐oxidative stress pathway
FOXO3↑,

238-

Api,

Apigenin inhibits TGF-β-induced VEGF expression in human prostate carcinoma cells via a Smad2/3- and Src-dependent mechanism

in-vitro,

Pca,

PC3

 25 uM

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

C4-2B

VEGF↓,
TGF-β↓,
Src↓,
FAK↓,
Akt↓,
SMAD2↓,
SMAD3↓,

1181-

Ash,

Withaferin A inhibits Epithelial to Mesenchymal Transition in Non-Small Cell Lung Cancer Cells

in-vitro,

Lung,

A549

0.5-4uM

in-vitro,

Lung,

H1299

TumCMig↓,
TumCI↓,
EMT↓,
p‑SMAD2↓,
p‑SMAD3↓,
p‑NF-kB↓,

2763-

BetA,

Betulinic Acid Inhibits the Stemness of Gastric Cancer Cells by Regulating the GRP78-TGF-β1 Signaling Pathway and Macrophage Polarization

in-vitro,

GC,

GRP78/BiP↓, The results indicated that BA inhibited not only GRP78-mediated stemness-related protein expression and GRP78-TGF-β-mediated macrophage polarization
TGF-β↓, BA Inhibits the Expression of GRP78, TGF-β1, and Stemness Markers in Human Gastric Cancer Cells
ChemoSen↑, BA is a promising candidate for clinical application in combination-chemotherapy targeting cancer stemness.
CSCs↓,
SMAD2↓, BA inhibited TGF-β/Smad2/3 signaling, TGF-β1 secretion, and OCT4 expression in a dose-dependent manner
SMAD3↓,
OCT4↓,

1105-

CEL,

Celecoxib inhibits the epithelial-to-mesenchymal transition in bladder cancer via the miRNA-145/TGFBR2/Smad3 axis

in-vitro,

BC,

COX2↓, Celecoxib, a selective cyclooxygenase-2 inhibitor
TumCP↓,
TumCMig↓,
TumCI↓,
EMT↓,
miR-145↑,
TGF-β↓,
SMAD3↓,

447-

CUR,

OXA,

Curcumin reverses oxaliplatin resistance in human colorectal cancer via regulation of TGF-β/Smad2/3 signaling pathway

vitro+vivo,

CRC,

HCT116

1, 2, 4, 8, 16, 32 and 64 μM, 48 h; 60 mg/kg, 3 weeks

4uM(Cur)+10uM(OXA)

p‑p65↓,
Bcl-2↓,
Casp3↑,
EMT↓,
p‑SMAD2↓,
p‑SMAD3↓,
N-cadherin↓,
TGF-β↓,
E-cadherin↑,
TumVol↓,
TumCMig↓,

1605-

EA,

Ellagic Acid and Cancer Hallmarks: Insights from Experimental Evidence

Review,

Var,

*BioAv↓, Within the gastrointestinal tract, EA has restricted bioavailability, primarily due to its hydrophobic nature and very low water solubility.
antiOx↓, strong antioxidant properties [12,13], anti-inflammatory effects
Inflam↓,
TumCP↓, numerous studies indicate that EA possesses properties that can inhibit cell proliferation
TumCCA↑, achieved this by causing cell cycle arrest at the G1 phase
cycD1/CCND1↓, reduction of cyclin D1 and E levels, as well as to the upregulation of p53 and p21 proteins
cycE/CCNE↓,
P53↑,
P21↑,
COX2↓, notable reduction in the protein expression of COX-2 and NF-κB as a result of this treatment
NF-kB↓,
Akt↑, suppressing Akt and Notch signaling pathways
NOTCH↓,
CDK2↓,
CDK6↓,
JAK↓, suppression of the JAK/STAT3 pathway
STAT3↓,
EGFR↓, decreased expression of epidermal growth factor receptor (EGFR)
p‑ERK↓, downregulated the expression of phosphorylated ERK1/2, AKT, and STAT3
p‑Akt↓,
p‑STAT3↓,
TGF-β↓, downregulation of the TGF-β/Smad3
SMAD3↓,
CDK6↓, EA demonstrated the capacity to bind to CDK6 and effectively inhibit its activity
Wnt/(β-catenin)↓, ability of EA to inhibit phosphorylation of EGFR
Myc↓, Myc, cyclin D1, and survivin, exhibited decreased levels
survivin↓,
CDK8↓, diminished CDK8 level
PKCδ↓, EA has demonstrated a notable downregulatory impact on the expression of classical isoenzymes of the PKC family (PKCα, PKCβ, and PKCγ).
tumCV↓, EA decreased cell viability
RadioS↑, further intensified when EA was combined with gamma irradiation.
eff↑, EA additionally potentiated the impact of quercetin in promoting the phosphorylation of p53 at Ser 15 and increasing p21 protein levels in the human leukemia cell line (MOLT-4)
MDM2↓, finding points to the ability of reduced MDM2 levels
XIAP↓, downregulation of X-linked inhibitor of apoptosis protein (XIAP).
p‑RB1↓, EA exerted a decrease in phosphorylation of pRB
PTEN↑, EA enhances the protein phosphatase activity of PTEN in melanoma cells (B16F10)
p‑FAK↓, reduced phosphorylation of focal adhesion kinase (FAK)
Bax:Bcl2↑, EA significantly increases the Bax/Bcl-2 rati
Bcl-xL↓, downregulates Bcl-xL and Mcl-1
Mcl-1↓,
PUMA↑, EA also increases the expression of Bcl-2 inhibitory proapoptotic proteins PUMA and Noxa in prostate cancer cells
NOXA↑,
MMP↓, addition to the reduction in MMP, the release of cytochrome c into the cytosol occurs in pancreatic cancer cells
Cyt‑c↑,
ROS↑, induction of ROS production
Ca+2↝, changes in intracellular calcium concentration, leading to increased levels of EndoG, Smac/DIABLO, AIF, cytochrome c, and APAF1 in the cytosol
Endoglin↑,
Diablo↑,
AIF↑,
iNOS↓, decreased expression of Bcl-2, NF-кB, and iNOS were observed after exposure to EA at concentrations of 15 and 30 µg/mL
Casp9↑, increase in caspase 9 activity in EA-treated pancreatic cancer cells PANC-1
Casp3↑, EA-induced caspase 3 activation and PARP cleavage in a dose-dependent manner (10–100 µmol/L)
cl‑PARP↑,
RadioS↑, EA sensitizes and reduces the resistance of breast cancer MCF-7 cells to apoptosis induced by γ-radiation
Hif1a↓, EA reduced the expression of HIF-1α
HO-1↓, EA significantly reduced the levels of two isoforms of this enzyme, HO-1, and HO-2, and increased the levels of sEH (Soluble epoxide hydrolase) in LnCap
HO-2↓,
SIRT1↓, EA-induced apoptosis was associated with reduced expression of HuR and Sirt1
selectivity↑, A significant advantage of EA as a potential chemopreventive, anti-tumor, or adjuvant therapeutic agent in cancer treatment is its relative selectivity
Dose∅, EA significantly reduced the viability of cancer cells at a concentration of 10 µmol/L, while in healthy cells, this effect was observed only at a concentration of 200 µmol/L
NHE1↓, EA had the capacity to regulate cytosolic pH by downregulating the expression of the Na+/H+ exchanger (NHE1)
Glycolysis↓, led to intracellular acidification with subsequent impairment of glycolysis
GlucoseCon↓, associated with a decrease in the cellular uptake of glucose
lactateProd↓, notable reduction in lactate levels in supernatant
PDK1?, inhibit pyruvate dehydrogenase kinase (PDK) -bind and inhibit PDK3
PDK1?,
ECAR↝, EA has been shown to influence extracellular acidosis
COX1↓, downregulation of cancer-related genes, including COX1, COX2, snail, twist1, and c-Myc.
Snail↓,
Twist↓,
cMyc↓,
Telomerase↓, EA, might dose-dependently inhibit telomerase activity
angioG↓, EA may inhibit angiogenesis
MMP2↓, EA demonstrated a notable reduction in the secretion of matrix metalloproteinase (MMP)-2 and MMP-9.
MMP9↓,
VEGF↓, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
Dose↝, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
PD-L1↓, EA downregulated the expression of the immune checkpoint PD-L1 in tumor cells
eff↑, EA might potentially enhance the efficacy of anti-PD-L1 treatment
SIRT6↑, EA exhibited statistically significant upregulation of sirtuin 6 at the protein level in Caco2 cells
DNAdam↓, increase in DNA damage

1618-

EA,

A comprehensive review on Ellagic acid in breast cancer treatment: From cellular effects to molecular mechanisms of action

Review,

BC,

TumCCA↑, suppresses the growth of BC cells by arresting the cell cycle in the G0/G1 phase,
TumCMig↓, suppresses migration, invasion, and metastatic
TumCI↓,
TumMeta↓,
Apoptosis↑, stimulates apoptosis in MCF-7 cells via TGF-β/Smad3 signaling axis
TGF-β↓,
SMAD3↓,
CDK6↓, inhibits CDK6 that is important in cell cycle regulation,
PI3K↓, inhibits the PI3K/AKT pathway
Akt↓,
angioG↓,
VEGFR2↓, reduces VEGFR-2 tyrosine kinase activity
MAPK↓,
NEDD9↓, downregulated protein 9 (NEDD-9)
NF-kB↓, EA suppressed NF-κB precursor protein p105
eff↑, They showed that the encapsulation of EA in biodegradable polymeric nanoparticles would improve the bioavailability after oral administration and also enhance the anticancer properties
eff↑, Chitosan nanoparticles and EA with high anticancer efficacy could be a suitable therapeutic strategy
RadioS↑, showed that the synergistic effect of EA combined with radiotherapy/chemotherapy resulted in increased DNA damage and apoptosis as well as decreased levels of MGMT expression
ChemoSen↑,
DNAdam↑,
eff↑, combination of Paclitaxel and EA has shown promise in inhibiting tumor growth and metastasis in experimental BC models.
*toxicity∅, 630 mg/kg is the LD50 of EA in the rat population.
*toxicity∅, no-observed adverse effect level of EA is 2000 mg/kg body weight

1110-

EA,

GEM,

Ellagic Acid Resensitizes Gemcitabine-Resistant Bladder Cancer Cells by Inhibiting Epithelial-Mesenchymal Transition and Gemcitabine Transporters

vitro+vivo,

Bladder,

TGF-β↓,
SMAD2↓,
SMAD3↓,
SMAD4↓,

1072-

EGCG,

Epigallocatechin gallate (EGCG) suppresses epithelial-Mesenchymal transition (EMT) and invasion in anaplastic thyroid carcinoma cells through blocking of TGF-β1/Smad signaling pathways

in-vitro,

Thyroid,

8505C

EMT↓,
TumCI↓,
TumCMig↓,
TGF-β↓,
p‑SMAD2↓,
p‑SMAD3↓,
SMAD4↓,

1323-

EMD,

Anticancer action of naturally occurring emodin for the controlling of cervical cancer

Review,

Cerv,

56.7 µmol/L

TumCCA↑, cell cycle arrest in the G2/M phase
DNAdam↑,
mTOR↓,
Casp3↑,
Casp8↑,
Casp9↑,
TGF-β↑,
SMAD3↓,
p‑SMAD4↓,
ROS↑,
MMP↓,
CXCR4↓,
HER2/EBBR2↓,
ER Stress↓,
TumAuto↑, can increase the level of autophagy in A549 lung cancer cells, but did not affect autophagy in healthy non-cancerous Ha CaT cells
NOTCH1↓,

817-

GAR,

Garcinol inhibits esophageal cancer metastasis by suppressing the p300 and TGF-β1 signaling pathways

vitro+vivo,

SCC,

KYSE150

5-15uM

mouse 20 mg/kg

vitro+vivo,

SCC,

KYSE450

HATs↓, Garcinol, a natural compound extracted from Gambogic genera, is a histone acetyltransferase (HAT) inhibitor
TumCCA↑,
Apoptosis↑,
TumCMig↓,
TumCI↓,
CBP↓,
p300↓,
TGF-β↓, suppressed TGF-β1-activated Smad and non-Smad pathway
Ki-67↓,
SMAD2↓,
SMAD3↓,

1117-

Gb,

Ginkgobiloba leaf extract mitigates cisplatin-induced chronic renal interstitial fibrosis by inhibiting the epithelial-mesenchymal transition of renal tubular epithelial cells mediated by the Smad3/TGF-β1 and Smad3/p38 MAPK pathways

vitro+vivo,

Kidney,

HK-2

rats

α-SMA↓,
COL1↓,
TGF-β↓, TGF-β1
SMAD2↓,
SMAD3↓,
p‑SMAD2↓,
p‑SMAD3↓, EGb inhibited cisplatin-induced EMT of renal tubular epithelial cells by downregulating the smad3/TGF-β1 and smad3/p38 MAPK pathways and ultimately effectively ameliorated CRIF.
p38↓,
p‑p38↓,
Vim↓,
TIMP1↓,
CTGF↓,
E-cadherin↑,
MMP1:TIMP1↑,

1118-

GSE,

Grape Seed Proanthocyanidins Inhibit Migration and Invasion of Bladder Cancer Cells by Reversing EMT through Suppression of TGF- β Signaling Pathway

in-vitro,

Bladder,

T24/HTB-9

in-vitro,

Bladder,

5637

TumCMig↓,
TumCI↓,
MMP2↓,
MMP9↓,
EMT↓,
N-cadherin↓,
Vim↓,
Slug↓,
E-cadherin↑,
ZO-1↑,
p‑SMAD2↓,
p‑SMAD3↓,
p‑Akt↓,
p‑ERK↓,
p‑p38↓,

2882-

HNK,

Honokiol Suppresses Perineural Invasion of Pancreatic Cancer by Inhibiting SMAD2/3 Signaling

in-vitro,

PC,

PANC1

TumCI↓, HNK can inhibit the invasion and migration of pancreatic cancer cells.
TumCMig↓,
p‑SMAD2↓, partially mediated by inhibition of SMAD2/3 phosphorylation.
p‑SMAD3↓,
EMT↓, HNK Inhibits Pancreatic Cancer Malignant Behaviors and EMT
N-cadherin↓, expression of N-cadherin and Vimentin was gradually downregulated, while HNK promoted the expression of E-cadherin in PANC-1
Vim↓,
E-cadherin↑,
Snail↓, HNK can inhibit breast cancer cell metastasis by blocking EMT through downregulating Snail/Slug protein translation
Slug↓,
Rho↓, Honokiol inhibits the migration of renal cell carcinoma through activation of the RhoA/ROCK/MLC signaling pathway
ROCK1↓,

2884-

HNK,

Honokiol inhibits EMT-mediated motility and migration of human non-small cell lung cancer cells in vitro by targeting c-FLIP

in-vitro,

Lung,

A549

in-vitro,

Lung,

H460

EMT↓, HNK inhibits EMT-mediated motility and migration of human NSCLC cells in vitro by targeting c-FLIP,
cFLIP↓,
N-cadherin↓, increased c-FLIP, N-cadherin (a mesenchymal marker), snail (a transcriptional modulator) and p-Smad2/3 expression, and decreased IκB levels in the cells; these changes were abrogated by co-treatment with HNK (30 μmol/L)
Snail↓,
p‑SMAD2↓,
p‑SMAD3↓,
IKKα↑,
TumCMig↓, HNK inhibits the migration of A549 and H460 cells induced by TNF-α+TGF-β1

4632-

HT,

Hydroxytyrosol inhibits cancer stem cells and the metastatic capacity of triple-negative breast cancer cell lines by the simultaneous targeting of epithelial-to-mesenchymal transition, Wnt/β-catenin and TGFβ signaling pathways

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

BT549

in-vitro,

BC,

SUM159

CSCs↓, HT reduced BCSCs self-renewal, ALDH+ (aldehyde dehydrogenase) and CD44+/CD24-/low subpopulations, tumor cell migration and invasion.
TumCMig↓,
TumCI↓,
β-catenin/ZEB1↓, HT suppressed Wnt/β-catenin signaling by decreasing p-LRP6, LRP6, β-catenin and cyclin D1 protein expression and the EMT markers SLUG, ZEB1, SNAIL and VIMENTIN.
Wnt↓,
p‑LRP6↓,
LRP6↓,
cycD1/CCND1↓,
EMT↓,
Slug↓,
Zeb1↓,
Snail↓,
Vim↓,
SMAD2↓, Finally, HT inhibited p-SMAD2/3 and SMAD2/3 in SUM159PT, BT549 and MDA-MB-231 cells, what was correlated with a less TGFβ activity.
SMAD3↓,
TGF-β↓,

1266-

LE,

Glycyrrhizin suppresses epithelial-mesenchymal transition by inhibiting high-mobility group box1 via the TGF-β1/Smad2/3 pathway in lung epithelial cells

in-vitro,

Lung,

A549

in-vitro,

Nor,

BEAS-2B

HMGB1↓,
EMT↓,
TumCMig↓,
p‑SMAD2↓,
p‑SMAD3↓,

4520-

MAG,

Magnolol Suppresses Pancreatic Cancer Development In Vivo and In Vitro via Negatively Regulating TGF-β/Smad Signaling

vitro+vivo,

PC,

PANC1

mice

Vim↓, Magnolol suppressed vimentin expression and facilitated E-cadherin expression.
E-cadherin↑,
EMT↓, Magnolol suppressed epithelial-mesenchymal-transition by increasing the expression level of E-cadherin and decreasing those of N-cadherin and vimentin.
N-cadherin↓,
p‑SMAD2↓, negatively regulating phosphorylation of Smad2/3.
p‑SMAD3↓,
TumCP↓, Magnolol can inhibit proliferation, migration and invasion in vivo and in vitro by suppressing the TGF-β signal pathway and EMT.
TumCMig↓,
TumCI↓,
TGF-β↓,

2643-

MCT,

Medium Chain Triglycerides enhances exercise endurance through the increased mitochondrial biogenesis and metabolism

Review,

Nor,

*Akt↑, increased mitochondrial biogenesis and metabolism is mediated through the activation of Akt and AMPK signaling pathways and inhibition of TGF-β signaling pathway.
*AMPK↓,
*TGF-β↓, MCT downregulates TGF-β signaling
eff↑, beneficial effect of dietary MCT in exercise performance through the increase of mitochondrial biogenesis and metabolism.
*BioEnh↑, Furthermore, addition of the combination of chilli and MCT to meals increased diet-induced thermogenesis by over 50% in heathy normal-weight humans
*ATP↑, a key regulator of energy metabolism and mitochondrial membrane ATP synthase (ATP5α) were significantly upregulated by MCT.
*PGC-1α↑, also observed a significant increase in protein level of PGC-1α and ATP5α
*p‑mTOR↑, increased levels in both total and phosphorylated Akt and mTOR
*SMAD3↓, a compensatory response of the huge reduction in Smad3.

3478-

MF,

One Month of Brief Weekly Magnetic Field Therapy Enhances the Anticancer Potential of Female Human Sera: Randomized Double-Blind Pilot Study

Trial,

BC,

in-vitro,

BC,

MCF-7

in-vitro,

Nor,

C2C12

TumCP↓, Female sera from the magnetic therapy group (n = 12) reduced breast cancer cell proliferation (16.1%), migration (11.8%) and invasion (28.2%) and reduced the levels of key EMT markers relative to the control sera
TumCMig↓,
TumCI↓,
*toxicity∅, The provision of week 5 or week 8 PEMF sera to MCF10A cells did not alter their viability, being comparable to that observed with the control sera (
TGF-β↓, The week 8 PEMF sera resulted in the significant downregulation of (A) TGFβR2, (B) TWIST, (C) SNAI1, (D) SNAI2 (Slug), (E) β-catenin and (F) Vimentin protein expressions, when compared to week 8 control sera
Twist↓,
Slug↓,
β-catenin/ZEB1↓,
Vim↓,
p‑SMAD2↓, Week 5 PEMF sera primarily reduced the phosphorylation of SMAD 2/3 as well as the expression of TWIST protein expression.
p‑SMAD3↓,
angioG↓, Week 8 PEMF-plasma showed significant reductions in angiogenic biomarkers, including Angiopoietin-2, BMP-9, Endoglin, PLGF, VEGF-A, and VEGF-D
VEGF↓,
selectivity↑, PEMF sera did not adversely alter the growth of non-malignant cells such as MCF10A (breast epithelial) and C2C12 (myogenic).
LIF↑, Similarly, LIF (leukemia inhibitory factor) was upregulated one week after the final PEMF treatment.

201-

MFrot,

MF,

Gradient Rotating Magnetic Fields Impairing F-Actin-Related Gene CCDC150 to Inhibit Triple-Negative Breast Cancer Metastasis by Inactivating TGF-β1/SMAD3 Signaling Pathway

in-vitro,

BC,

MDA-MB-231

 5 Hz, 0.41 T

in-vitro,

BC,

BT549

in-vitro,

BC,

MDA-MB-468

CCDC150↓, magnetic field response gene
TGF-β↓,
SMAD3↓,

1128-

Myr,

Myricetin suppresses TGF-β-induced epithelial-to-mesenchymal transition in ovarian cancer

vitro+vivo,

Ovarian,

MAPK↓,
ERK↓,
PI3K↓,
Akt↓,
p‑PARP↑,
cl‑Casp3↑,
Bax:Bcl2↑,
TumCMig↓,
SMAD3↓,

1131-

PI,

Piperlongumine‑loaded nanoparticles inhibit the growth, migration and invasion and epithelial‑to‑mesenchymal transition of triple‑negative breast cancer cells

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

BT549

TumCG↓,
tumCV↓,
TumCMig↓,
TumCI↓,
MMP2↓,
Slug↓,
N-cadherin↓,
β-catenin/ZEB1↓,
SMAD3↓,
E-cadherin↑,
EMT↓,

3098-

RES,

Regulation of Cell Signaling Pathways and miRNAs by Resveratrol in Different Cancers

Review,

Var,

NOTCH2↓, resveratrol has been reported to target multiple proteins in ovarian cancer, markedly reducing NOTCH2 and HES1 in OVCAR-3 and CAOV-3 cells
Wnt↓, In CAOV-3 cells, resveratrol downregulated WNT2 and reduced the nuclear accumulation of β-catenin
β-catenin/ZEB1↓,
p‑SMAD2↓, Resveratrol effectively inhibits SMAD proteins
p‑SMAD3↓, Resveratrol has been reported to reduce phosphorylated-SMAD2/3 in colorectal cancer LoVo cells
PTCH1↓, PTCH, SMO, and GLI-1 were also inhibited in resveratrol-treated colorectal cancer HCT116 cells
Smo↓,
Gli1↓,
E-cadherin↑, resveratrol upregulated E-cadherin
NOTCH⇅, Although some reports document efficient inhibition of different proteins of the NOTCH pathway by resveratrol to inhibit cancer, there are conflicting reports that resveratrol can activate the NOTCH pathway, leading to its anticancer activity.
TAC?,
NKG2D↑, Resveratrol has been found to increase the cell-surface expression of NKG2D ligands and DR4 along
DR4↑,
survivin↓, Resveratrol dose-dependently downregulated survivin in HepG2 cells.
DR5↑, resveratrol upregulated DR4, DR5, Bax, and p27(/KIP1) and inhibited the expression of cyclin D1 and Bcl-2
BAX↑,
p27↑,
cycD1/CCND1↓,
Bcl-2↓,
STAT3↓, Resveratrol exerts inhibitory effects on the constitutive activation of STAT3 and STAT5.
STAT5↓,
JAK↓, Resveratrol has also been shown to prevent the activation of JAK,
DNAdam↑, Resveratrol induced DNA damage, as evidenced by the presence of multiple γ-H2AX foci after treatment with 25 μM resveratrol.
γH2AX↑,

3092-

RES,

Resveratrol in breast cancer treatment: from cellular effects to molecular mechanisms of action

Review,

BC,

MDA-MB-231

Review,

BC,

MCF-7

TumCP↓, The anticancer mechanisms of RES in regard to breast cancer include the inhibition of cell proliferation, and reduction of cell viability, invasion, and metastasis.
tumCV↓,
TumCI↓,
TumMeta↓,
*antiOx↑, antioxidative, cardioprotective, estrogenic, antiestrogenic, anti-inflammatory, and antitumor properties it has been used against several diseases, including diabetes, neurodegenerative diseases, coronary diseases, pulmonary diseases, arthritis, and
*cardioP↑,
*Inflam↓,
*neuroP↑,
*Keap1↓, RES administration resulted in a downregulation of Keap1 expression, therefore, inducing Nrf2 signaling, and leading to a decrease in oxidative damage
*NRF2↑,
*ROS↓,
p62↓, decrease the severity of rheumatoid arthritis by inducing autophagy via p62 downregulation, decreasing the levels of interleukin-1β (IL-1β) and C-reactive protein as well as mitigating angiopoietin-1 and vascular endothelial growth factor (VEGF) path
IL1β↓,
CRP↓,
VEGF↓,
Bcl-2↓, RES downregulates the levels of Bcl-2, MMP-2, and MMP-9, and induces the phosphorylation of extracellular-signal-regulated kinase (ERK)/p-38 and FOXO4
MMP2↓,
MMP9↓,
FOXO4↓,
POLD1↓, The in vivo experiment involving a xenograft model confirmed the ability of RES to reduce tumor growth via POLD1 downregulation
CK2↓, RES reduces the expression of casein kinase 2 (CK2) and diminishes the viability of MCF-7 cells.
MMP↓, Furthermore, RES impairs mitochondrial membrane potential, enhances ROS generation, and induces apoptosis, impairing BC progression
ROS↑,
Apoptosis↑,
TumCCA↑, RES has the capability of triggering cell cycle arrest at S phase and reducing the number of 4T1 BC cells in G0/G1 phase
Beclin-1↓, RES administration promotes cytotoxicity of DOX against BC cells by downregulating Beclin-1 and subsequently inhibiting autophagy
Ki-67↓, Reducing the Ki-67
ATP↓, RES’s administration is responsible for decreasing ATP production and glucose metabolism in MCF-7 cells.
GlutMet↓,
PFK↓, RES decreased PFK activity, preventing glycolysis and glucose metabolism in BC cells and decreasing cellular growth rate
TGF-β↓, RES (12.5–100 µM) inhibited TGF-β signaling and reduced the expression levels of its downstream targets that include Smad2 and Smad3 and as a result impaired the progression of BC cells.
SMAD2↓,
SMAD3↓,
Vim?, a significant decrease in the levels of vimentin, Snail1 and Slug occurred, while E-cadherin levels increased to suppress EMT and metastasis of BC cells.
Snail↓,
Slug↓,
E-cadherin↑,
EMT↓,
Zeb1↓, a significant decrease in the levels of vimentin, Snail1 and Slug occurred, while E-cadherin levels increased to suppress EMT and metastasis of BC cells.
Fibronectin↓,
IGF-1↓, RES administration (10 and 20 µM) impaired the migration and invasion of BC cells via inhibiting PI3K/Akt and therefore decreasing IGF-1 expression and preventing the upregulation of MMP-2
PI3K↓,
Akt↓,
HO-1↑, The activation of heme oxygenase-1 (HO-1) signaling by RES reduced MMP-9 expression and prevented metastasis of BC cells
eff↑, RES-loaded gold nanoparticles were found to enhance RES’s ability to reduce MMP-9 expression as compared to RES alone
PD-1↓, RES inhibited PD-1 expression to promote CD8+ T cell activity and enhance Th1 immune responses.
CD8+↑,
Th1 response↑,
CSCs↓, RES has the ability to target CSCs in various tumors
RadioS↑, RES in reversing drug resistance and radio resistance.
SIRT1↑, RES administration (12.5–200 µmol/L) promotes sensitivity of BC cells to DOX by increasing Sirtuin 1 (SIRT1) expression
Hif1a↓, downregulating HIF-1α expression, an important factor in enhancing radiosensitivity
mTOR↓, mTOR suppression

878-

RES,

Resveratrol suppresses epithelial-to-mesenchymal transition in colorectal cancer through TGF-β1/Smads signaling pathway mediated Snail/E-cadherin expression

vitro+vivo,

CRC,

LoVo

12.5uM, 150 mg/Kg

mice

TumMeta↓,
E-cadherin↑,
Vim↓,
TGF-β↓,
SMAD2↓,
EMT↓,
SMAD3↓,

1134-

SANG,

Sanguinarine inhibits epithelial–mesenchymal transition via targeting HIF-1α/TGF-β feed-forward loop in hepatocellular carcinoma

in-vitro,

HCC,

HepG2

0.4-50uM

4uM

impairs the proliferation of nine kinds of HCC cell lines

in-vitro,

HCC,

Hep3B

4.5uM

in-vitro,

HCC,

HUH7

3uM

Hif1a↓,
EMT↓,
Snail↓,
PI3K↓,
Akt↓,
SMAD2↓,
SMAD3↓,

1133-

SM,

Salvianolic Acid A, a Component of Salvia miltiorrhiza, Attenuates Endothelial-Mesenchymal Transition of HPAECs Induced by Hypoxia

in-vitro,

Nor,

HPAECs

*ROS↓,
*p‑Smad1↑,
*p‑SMAD5↑,
*SMAD2↓,
*SMAD3↓,
*p‑ERK↓,
*p‑Cofilin↓,

1138-

TQ,

Thymoquinone inhibits epithelial-mesenchymal transition in prostate cancer cells by negatively regulating the TGF-β/Smad2/3 signaling pathway

in-vitro,

Pca,

DU145

in-vitro,

Pca,

PC3

TumMeta↓,
EMT↓, thymoquinone reversed EMT
E-cadherin↑,
Vim↓,
Slug↓,
TGF-β↓,
SMAD2↓,
SMAD3↓,

Showing Research Papers: 1 to 30 of 30

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 30

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 1,
Total Targets: 185

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Keap1↓, 1, NRF2↑, 1, ROS↓, 2,

Mitochondria & Bioenergetics ⓘ

ATP↑, 1, PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↓, 1,

Cell Death ⓘ

Akt↑, 1,

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↓, 1, p‑mTOR↑, 1,

Migration ⓘ

p‑Cofilin↓, 1, p‑Smad1↑, 1, SMAD2↓, 1, SMAD3↓, 2, p‑SMAD5↑, 1, TGF-β↓, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioEnh↑, 1,

Functional Outcomes ⓘ

cardioP↑, 1, neuroP↑, 1, toxicity∅, 3,
Total Targets: 22

Scientific Paper Hit Count for: SMAD3, SMAD3

3 Ellagic acid
3 Resveratrol
2 Honokiol
2 Magnetic Fields
1 Andrographis
1 Apigenin (mainly Parsley)
1 Ashwagandha(Withaferin A)
1 Betulinic acid
1 Celecoxib
1 Curcumin
1 Oxaliplatin
1 Gemcitabine (Gemzar)
1 EGCG (Epigallocatechin Gallate)
1 Emodin
1 Garcinol
1 Ginkgo biloba
1 Grapeseed extract
1 HydroxyTyrosol
1 Licorice
1 Magnolol
1 MCToil
1 Magnetic Field Rotating
1 Myricetin
1 Piperine
1 Sanguinarine
1 Salvia miltiorrhiza
1 Thymoquinone

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#:556  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

SMAD3 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

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