Smad1 Cancer Research Results

Smad1, Smad1: Click to Expand ⟱
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SMAD1 is a member of the SMAD family of proteins that are key intracellular mediators of the bone morphogenetic protein (BMP) signaling pathway. BMP/SMAD signaling plays a variety of roles in cell differentiation, proliferation, apoptosis, and migration.

In some cancers, altered SMAD1 expression has been reported. For example, reduced expression can compromise the tumor-suppressive BMP signaling in some contexts, potentially allowing for unchecked cell proliferation.
In other scenarios, particularly where BMP signaling promotes tumor progression or metastasis, elevated SMAD1 might be associated with a more aggressive phenotype.

In cancers where SMAD1 functions predominantly as a tumor suppressor (via proper BMP signaling), lower levels of SMAD1 might be associated with a poorer prognosis.
Conversely, in tumors where BMP signaling contributes to invasion or metastasis, higher SMAD1 expression may correlate with aggressive disease and worse outcomes.


Scientific Papers found: Click to Expand⟱
6784- EGCG,    Dietary (−)-Epigallocatechin Gallate (EGCG): State-of-the-Art Advances in Bioactivities, Bioavailability Enhancement Strategies, and Applications in Nutrition and Health
- Review, Nor, NA
*antiOx↑, bioactivities of EGCG, including its antioxidant, anti-inflammatory, anticancer, cardiovascular protective, metabolic regulatory, neuroprotective, gut microbiota-modulating, and antimicrobial properties.
*Inflam↓,
*AntiCan↑,
*cardioP↑,
*neuroP↑,
*GutMicro↑,
*AntiBio↑,
*ROS↓, Figure 1, anti inflammatory
*TNF-α↓,
*IL6↓,
TumCP↓,
*LDL↓, cardioprotective
*NO↓,
*Obesity↓, Metabolic syndrome
*p‑tau↓, nervous system
*Aβ↓,
*NRF2↑, , EGCG has been shown to activate the Keap1/P62/Nrf2 signaling pathway,
*SOD↑, upregulation of endogenous antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione peroxidase, indirectly diminishing the levels of intracellular oxygen free radicals
*Catalase↑,
*GPx↑,
*NLRP3↓, EGCG also restores autophagy levels, suppresses the activation of the NLRP3 inflammasome by inhibiting the mammalian target of rapamycin signaling pathway
*mTOR↓,
TumCCA↑, Cancer: induce cell cycle arrest and inhibit tumor cell proliferation
NRF2↓, EGCG inhibits CCL5-stimulated lung cancer cell proliferation by down-regulating Nrf2 expression
Apoptosis↑, Inducing Apoptosis in Cancer Cells
SIRT1↓, EGCG activates the mitochondrial apoptotic pathway by downregulating SIRT1 expression to modulate the SIRT1-p53 axis
miR-25-5p↓, In breast cancer, EGCG induces apoptosis by inhibiting miR-25 expression and elevating PARP, pre-caspase-3 and pre-caspase-9 protein levels
PARP↑,
Casp3↑,
Casp9↑,
ER Stress↑, in multiple myeloma, EGCG promotes apoptosis by activating the endoplasmic reticulum stress pathway
TumAuto↑, EGCG induces autophagic cell death in breast cancer cells by retaining YAP1 in the cytoplasm and promoting the assembly of the CHMP2B-VPS4B complex
EMT↓, EGCG has been demonstrated to inhibit EMT, invasion, and migration by blocking the TGFβ/Smad signaling pathway
TumCI↓,
TumCMig↓,
TGF-β↓,
Smad1↓,
STAT3↓, EGCG can directly bind to STAT3, reducing nuclear localization and inhibiting the transcription of PLXNC1.
VEGF↓, widely believed that EGCG can block this process by reducing the expression of vascular endothelial growth factor, a key factor in angiogenesis,
angioG↓, The inhibition of angiogenic mimicry by EGCG through the Twist/VE-calmodulin/AKT pathway has also been demonstrated in prostate cancer cells
Imm↑, Acting as an Immunomodulator
EGFR↓, EGCG possesses the ability to interact with EGFR and inhibit activity, strengthening the anticancer evidence for EGCG
*GutMicro↑, EGCG can regulate the balance of gut flora. For example, EGCG can inhibit the growth of harmful bacteria such as Escherichia coli and Salmonella, while promoting the proliferation of probiotics like Bifidobacterium and Lactobacillus
*Bacteria↓, Antibacterial and Antiviral Properties of EGCG
*AntiViral↑,
*BioAv↓, EGCG, its low bioavailability in the human body limits clinical efficacy.
*BioAv↑, Nanotechnology strategy of EGCG.
*eff↑, Co-encapsulation assay of EGCG with quercetin shows that the two synergistically enhanced the antioxidant capacity of EGCG
*BioAv↑, Combining EGCG with resveratrol increases its solubility and significantly improves its absorption in the small intestine.
eff↑, combination of EGCG and curcumin inhibits the activity of metabolic enzymes, reduces the rate of metabolism in the liver and enhances its antitumor efficacy
ChemoSen↑, synergistic effects of EGCG combined with chemotherapeutic agents such as 5-fluorouracil, celecoxib, cisplatin, and tamoxifen have also been reported
*toxicity↝, The European Food Safety Authority notes in scientific opinion that daily oral doses of 800 mg or higher of EGCG represent a common starting point for observed cases of liver injury

6580- EU,    Eurycomanone Blocks TGF-β1-Induced Epithelial-to-Mesenchymal Transition, Migration, and Invasion Pathways in Human Non-Small Cell Lung Cancer Cells by Targeting Smad and Non-Smad Signaling
- in-vitro, Lung, A549 - in-vitro, Lung, Calu-1
TumCMig↓, ECN significantly suppressed the migration of both TGF-β1-induced A549 and Calu-1 cells.
MMP2↓, decreased the secretion of MMP-2 from these cancer cells.
EMT↓, ECN Suppresses TGF-β1-Induced Epithelial-to-Mesenchymal Transition of NSCLC Cells
E-cadherin↑, ECN significantly restored the expression of E-cadherin by inhibiting the Akt signaling pathway.
Akt↓,
N-cadherin↓, in Calu-1, ECN reduced the aggressive phenotype by decreasing the expression of the mesenchymal protein N-cadherin and inhibiting the TGF-β1/Smad pathway.
TGF-β↓,
Smad1↓,

4926- PEITC,    PEITC inhibits the invasion and migration of colorectal cancer cells by blocking TGF-β-induced EMT
- in-vitro, CRC, SW48
TumCI↓, PEITC inhibits the invasion and migration of colorectal cancer cells.
TumCMig↓,
EMT↓, PEITC suppresses the EMT of colorectal cancer cells
Smad1↓, PEITC blocks the TGF-β1/Smad signaling pathway and TGF-β1 induced EMT.
AntiCan↑, PEITC exerts remarkable anti-cancer effects in several types of cancer, such as gastric cancer [20], lung cancer [21], prostate cancer [22], melanoma [23], breast cancer [24] and CRC
Snail↓, (SNAIL1, SLUG, ZEB1 and ZEB2). As shown in the Fig. 3B, PEITC treatment downregulated the expression levels of these four genes
Slug↓,
Zeb1↓,
ZEB2↓,
TGF-β1↓, PEITC significantly decreased the levels of TGF-β1 in SW480 cells.
eff↑, A recent study demonstrated the chemopreventive role of PEITC and curcumin in prostate cancer xenografts
E-cadherin↑, PEITC was found to upregulate epithelial markers (E-cadherin) and downregulate mesenchymal markers (N-cadherin, Vimentin) of CRC cells.
N-cadherin↓,
Vim↓,

4657- RES,    Resveratrol, cancer and cancer stem cells: A review on past to future
- Review, Var, NA
CSCs↓, RSV is reported to regulate all the major CSC signaling pathways, but exact mechanisms of its interactions are not clearly understood
CD133↓, CD133(+) cells ↓
Shh↓, Sonic hedgehog (Shh) ↓
Twist↓, GBM Stem cell marker expression: Twist ↓, Snail↓, Slug ↓, MMP-2 ↓, MMP-9 ↓, Smad ↓
Snail↓,
MMP2↓,
MMP9↓,
Smad1↓,
CD44↓, CSC marker proteins: CD44, CD133, ALDH1A1, Oct-4, Nanog ↓
ALDH1A1↓,
OCT4↓,
Nanog↓,
STAT3↓, STAT3 ↓
survivin↓, Survivin, cyclin D1, Cox-2 and c-Myc ↓
cycD1/CCND1↓,
COX2↓,
cMyc↓,


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(tgid=1)

NRF2↓, 1,  

Core Metabolism/Glycolysis(tgid=4)

cMyc↓, 1,   SIRT1↓, 1,  

Cell Death(tgid=5)

Akt↓, 1,   Apoptosis↑, 1,   Casp3↑, 1,   Casp9↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction(tgid=6)

miR-25-5p↓, 1,  

Protein Folding & ER Stress(tgid=8)

ER Stress↑, 1,  

Autophagy & Lysosomes(tgid=9)

TumAuto↑, 1,  

DNA Damage & Repair(tgid=10)

PARP↑, 1,  

Cell Cycle & Senescence(tgid=11)

cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

ALDH1A1↓, 1,   CD133↓, 1,   CD44↓, 1,   CSCs↓, 1,   EMT↓, 3,   Nanog↓, 1,   OCT4↓, 1,   Shh↓, 1,   STAT3↓, 2,  

Migration(tgid=13)

E-cadherin↑, 2,   MMP2↓, 2,   MMP9↓, 1,   N-cadherin↓, 2,   Slug↓, 1,   Smad1↓, 4,   Snail↓, 2,   TGF-β↓, 2,   TGF-β1↓, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 1,   Twist↓, 1,   Vim↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,  

Angiogenesis & Vasculature(tgid=14)

angioG↓, 1,   EGFR↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

COX2↓, 1,   Imm↑, 1,  

Drug Metabolism & Resistance(tgid=21)

ChemoSen↑, 1,   eff↑, 2,  

Clinical Biomarkers(tgid=22)

EGFR↓, 1,  

Functional Outcomes(tgid=23)

AntiCan↑, 1,  
Total Targets: 48

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0)

AntiBio↑, 1,  

Redox & Oxidative Stress(tgid=1)

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,  

Core Metabolism/Glycolysis(tgid=4)

LDL↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

mTOR↓, 1,  

Angiogenesis & Vasculature(tgid=14)

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

IL6↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Synaptic & Neurotransmission(tgid=18)

p‑tau↓, 1,  

Protein Aggregation(tgid=19)

Aβ↓, 1,   NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21)

BioAv↓, 1,   BioAv↑, 2,   eff↑, 1,  

Clinical Biomarkers(tgid=22)

GutMicro↑, 2,   IL6↓, 1,  

Functional Outcomes(tgid=23)

AntiCan↑, 1,   cardioP↑, 1,   neuroP↑, 1,   Obesity↓, 1,   toxicity↝, 1,  

Infection & Microbiome(tgid=24)

AntiViral↑, 1,   Bacteria↓, 1,  
Total Targets: 28

Scientific Paper Hit Count for: Smad1, Smad1
1 EGCG (Epigallocatechin Gallate)
1 Eurycomanone
1 Phenethyl isothiocyanate
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
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1011  State#:%  Dir#:1
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