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⟱
5536- BBM,    Regulation of Cell-Signaling Pathways by Berbamine in Different Cancers
- Review, Var, NA
JAK↝, In this review, we comprehensively analyze how berbamine modulates deregulated pathways (JAK/STAT, CAMKII/c-Myc) in various cancers.
STAT3↓, Berbamine physically interacted with STAT3 and inhibited its activation [8].
p‑CaMKII ↓, An orally administered, bioactive small molecule analog of berbamine, tosyl chloride-berbamine (TCB), considerably reduced phosphorylated levels of CaMKIIγ
TGF-β↑, berbamine induces activation of the TGF/SMAD pathway for the effective inhibition of cancer progression.
Smad1↑,
ChemoSen↑, Berbamine enhanced the chemosensitivity of gefitinib against PANC-1 and MIA PaCa-2 cancer cells [8].
RadioS↑, Moreover, berbamine and radiation effectively induced a regression of the tumors in mice subcutaneously injected with FaDu cells [10].
TumCI↓, berbamine-GMO-TPGS nanoparticles showed superior cellular toxicity, as well as an inhibition of migration and invasion in metastatic breast cancer MDA-MB-231,
TumCMig↓,
ROS↑, Berbamine increased the intracellular ROS levels via the downregulation of antioxidative genes such as NRF2, SOD2, GPX-1 and HO-1.
NRF2↓,
SOD2↓,
GPx1↓,
HO-1↓,

2685- BBR,    Berberine induces neuronal differentiation through inhibition of cancer stemness and epithelial-mesenchymal transition in neuroblastoma cells
- in-vitro, neuroblastoma, NA
CSCs↓, Berberine attenuated cancer stemness markers CD133, β-catenin, n-myc, sox2, notch2 and nestin.
CD133↓,
β-catenin/ZEB1↓,
n-MYC↓,
SOX2↓,
NOTCH2↓,
Nestin↓,
TumCCA↑, Berberine potentiated G0/G1 cell cycle arrest by inhibiting proliferation, cyclin dependent kinases and cyclins resulting in apoptosis through increased bax/bcl-2 ratio.
TumCP↓,
CDK1↓,
Cyc↓,
Apoptosis↑,
Bax:Bcl2↑,
NCAM↓, The induction of NCAM and reduction in its polysialylation indicates anti-migratory potential which is supported by down regulation of MMP-2/9.
MMP2↓,
MMP9↓,
*Smad1↑, It increased epithelial marker laminin and smad and increased Hsp70 levels also suggest its protective role.
*HSP70/HSPA5↑,
*LAMs↑,

2760- BetA,    A Review on Preparation of Betulinic Acid and Its Biological Activities
- Review, Var, NA - Review, Stroke, NA
AntiTum↑, BA is considered a future promising antitumor compound
Cyt‑c↑, BA stimulated mitochondria to release cytochrome c and Smac and cause further apoptosis reactions
Smad1↑,
Sepsis↓, Administration of 10 and 30 mg/kg of BA significantly improved survival against sepsis and attenuated lung injury.
NF-kB↓, BA inhibited nuclear factor-kappa B (NF-κB) expression in the lung and decreased levels of cytokine, intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1) and matrix metalloproteinase-9 (MMP-9)
ICAM-1↓,
MCP1↓,
MMP9↓,
COX2↓, In hPBMCs, BA suppressed cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PEG2) production by inhibiting extracellular regulated kinase (ERK) and Akt phosphorylation and thereby modulated the NF-κB signaling pathway
PGE2↓,
ERK↓,
p‑Akt↓,
*ROS↓, BA significantly decreased the mortality of mice against endotoxin shock and inhibited the production of PEG2 in two of the most susceptible organs, lungs and livers [80]. Moreover, BA reduced reactive oxygen species (ROS) formation
*LDH↓, and the release of lactate dehydrogenase
*hepatoP↑, hepatoprotective effect of BA from Tecomella undulata.
*SOD↑, Pretreatment of BA prevented the depletion of hepatic antioxidants superoxide dismutase (SOD) and catalase (CAT), reduced glutathione (GSH) and ascorbic acid (AA) and decreased the CCl4-induced LPO level
*Catalase↑,
*GSH↑,
*AST↓, A also attenuated the elevation of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) plasma level,
*ALAT↓,
*RenoP↑, BA also exhibits renal-protective effects. Renal fibrosis is an end-stage renal disease symptom that develops from chronic kidney disease (CKD).
*ROS↓, BA protected against this ischemia-reperfusion injury in a mice model by enhancing blood flow and reducing oxidative stress and nitrosative stress
*α-SMA↓, Moreover, BA reduced the expression of α-smooth muscle actin (α-SMA) and collagen-I

4950- PEITC,    Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential
- vitro+vivo, Pca, PC3
MMP↓, The PEITC-induced cell death in PC-3 cells was associated with disruption of the mitochondrial membrane potential, release of apoptogenic molecules (cytochrome c and Smac/DIABLO) from mitochondria to the cytosol and generation of reactive oxygen spe
Cyt‑c↑,
Smad1↑,
Diablo↑,
ROS↑,

3192- SFN,    Transcriptome analysis reveals a dynamic and differential transcriptional response to sulforaphane in normal and prostate cancer cells and suggests a role for Sp1 in chemoprevention
- in-vitro, Pca, PC3
Sp1/3/4↓, Sp1 protein was significantly decreased by SFN treatment in prostate cancer cells . Because SFN decreased the expression of Sp1, and to a lesser extent Sp3
selectivity↑, SFN alters gene expression differentially in normal and cancer cells with key targets in chemopreventive processes, making it a promising dietary anti-cancer agent.
NRF2↑, through the induction of phase 2 enzymes via Keap1-Nrf2 signaling
HDAC↓, SFN also inhibits the activity and/or expression of genes that regulate epigenetic mechanisms including histone deactylases (HDACs) and DNA methyltransferases (DNMTs) in cancer cells
DNMTs↓,
TumCCA↑, 15 μM SFN treatment induces cell cycle arrest at the G1 phase and only modestly increases apoptosis
selectivity↑, Normal prostate epithelial cells (PREC) do not undergo cell cycle arrest or apoptosis in response to this SFN treatment
HO-1↑, In all cell lines and time points, HO1 and NQO1 were identified as significantly upregulated by SFN
NQO1↑,
CDK2↓, MX non-receptor tyrosine kinase (BMX), cyclin-dependent kinase 2 (CDK2), and polo-like kinase 1 (PLK1) had decreased expression with SFN treatment
TumCP↓, suppression of Sp1 expression decreased prostate cancer cells proliferation.
BID↑, SFN treatment produced a significant increase in the expression of the apoptosis related genes Bid, Smac/Diablo, and ICAD only in PC-3 cells (
Smad1↑,
Diablo↑,
ICAD↑,
Cyt‑c↑, It also increased the expression of cytochrome c, c-IAP1, and HSP27 in PC-3 cells while it decreased expression in PREC cells.
IAP1↑,
HSP27↑,
*Cyt‑c↓,
*IAP1↓,
*HSP27↓,
survivin↓, In these studies, inhibition of Sp1 is associated with inhibition of the cancer promoting genes survivin, CDK4, VEGF and the androgen receptor.
CDK4↓,
VEGF↓,
AR↓,

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↓,

3120- VitC,    Upregulation of TET activity with ascorbic acid induces epigenetic modulation of lymphoma cells
- in-vitro, lymphoma, NA
TET2↑, ascorbic acid (AA) is a cofactor for TET with a binding site at the catalytic domain, and enhances TET activity
Smad1↑, AA treatment increased the expression of SMAD1, a tumor suppressor gene known to be suppressed by methylation, and increased chemosensitivity of lymphoma cells.
ChemoSen↑,
other↝, AA treatment produced a progressive decrease in DNA methylation and an increase in the hydroxymethylation fraction in a dose-dependent manner, correlating with the increase in TET activity


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GPx1↓, 1,   HO-1↓, 1,   HO-1↑, 1,   NQO1↑, 1,   NRF2↓, 1,   NRF2↑, 1,   ROS↑, 2,   SOD2↓, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   Bax:Bcl2↑, 1,   BID↑, 1,   Cyt‑c↑, 3,   Diablo↑, 2,   IAP1↑, 1,   ICAD↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction ⓘ

p‑CaMKII ↓, 1,   Sp1/3/4↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Protein Folding & ER Stress ⓘ

HSP27↑, 1,  

DNA Damage & Repair ⓘ

DNMTs↓, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 1,   Cyc↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CSCs↓, 1,   ERK↓, 1,   HDAC↓, 1,   n-MYC↓, 1,   Nestin↓, 1,   NOTCH2↓, 1,   SOX2↓, 1,   STAT3↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 2,   NCAM↓, 1,   Smad1↑, 5,   TGF-β↑, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   ICAM-1↓, 1,   JAK↝, 1,   MCP1↓, 1,   NF-kB↓, 1,   PGE2↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   RadioS↑, 1,   selectivity↑, 2,   TET2↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,  

Infection & Microbiome ⓘ

Sepsis↓, 1,  
Total Targets: 61

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

Catalase↑, 1,   GSH↑, 1,   ROS↓, 3,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   LDH↓, 1,  

Cell Death ⓘ

Cyt‑c↓, 1,   IAP1↓, 1,  

Protein Folding & ER Stress ⓘ

HSP27↓, 1,   HSP70/HSPA5↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↓, 1,  

Migration ⓘ

p‑Cofilin↓, 1,   LAMs↑, 1,   Smad1↑, 1,   p‑Smad1↑, 1,   SMAD2↓, 1,   SMAD3↓, 1,   p‑SMAD5↑, 1,   α-SMA↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,   RenoP↑, 1,  
Total Targets: 24

Scientific Paper Hit Count for: Smad1, Smad1
1 Berbamine
1 Berberine
1 Betulinic acid
1 Phenethyl isothiocyanate
1 Sulforaphane (mainly Broccoli)
1 Salvia miltiorrhiza
1 Vitamin C (Ascorbic Acid)
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#:2
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