TGF-β1 Cancer Research Results

TGF-β1, Transforming Growth Factor-Beta 1: Click to Expand ⟱
Source:
Type:
TGF-β1 is one of three TGF-β ligands (β1, β2, β3) that initiate the TGF-β signaling cascade.
In the context of cancer, TGF-β1 plays a dual role:
Tumor Suppressor in Early Stages: In normal and early-stage tumor cells, TGF-β1 typically inhibits cell proliferation, induces apoptosis, and maintains tissue homeostasis.
Tumor Promoter in Advanced Stages: As cancer progresses, TGF-β1 often promotes epithelial-to-mesenchymal transition (EMT), enhances invasiveness, contributes to immune evasion, and fosters a pro-metastatic microenvironment.

Role in Early Tumorigenesis: Acts as a tumor suppressor via growth arrest and apoptosis.
Role in Advanced Cancers: Promotes EMT, invasion, metastasis, and immune suppression.
Expression in Cancer Types: Increased in advanced/ aggressive tumors in many cancer types.
Prognostic Implications Elevated TGF-β1: associated with poor prognosis in several cancers due to its pro-tumorigenic functions.
Therapeutic Targeting Blocking TGF-β1 activity (via antibodies or ligand traps) to reduce its tumor-promoting actions.
Scientific Papers found: Click to Expand⟱
5444- AG,    A Systematic Review of Phytochemistry, Pharmacology and Pharmacokinetics on Astragali Radix: Implications for Astragali Radix as a Personalized Medicine
- Review, Var, NA
*Imm↑, AR possesses various biological functions, including potent immunomodulation, antioxidant, anti-inflammation and antitumor activities.
*antiOx↑,
*Inflam↓,
AntiTum↑,
eff↑, characteristics of increasing curative effect and reducing the toxicity of chemotherapeutic drugs [11 , 118].
chemoP↑,
Dose↝, main bioactive compounds responsible for the anti-cancer effects of AR mainly include formononetin, AS-IV and APS. S
TumCMig↓, AS-IV could inhibit the migration and proliferation of non-small cell lung cancer (NSCLC
TumCP↓,
Akt↓, h via inhibition of the Akt/GSK-3β/β-catenin signaling axis.
GSK‐3β↓,
MMP2↓, downregulating the expression of matrix metalloproteases (MMP)-2 and -9
MMP9↓,
EMT↓, AS-IV could inhibit TGF-B1 induced EMT through inhibition of PI3K/AKT/NF-KB
PI3K↓,
Akt↓,
NF-kB↓,
Inflam↓,
TGF-β1↓,
TNF-α↓,
IL6↓,
Fas↓, reduced FAS/FasL
FasL↓,
NOTCH1↓, decressing notch1
JNK↓, inactivating JNK pathway [145]
TumCG↓, The results showed that the AR water extract could inhibit the growth of colorectal cancer in vivo without apparent toxicity and side effect, which suggests that AR is a potential therapeutic drug for colorectal cancer

2662- AL,    Allicin inhibits tubular epithelial-myofibroblast transdifferentiation under high glucose conditions in vitro
- in-vitro, Nor, HK-2
*α-SMA↓, Allicin partially reversed the high-glucose-induced increase in α-SMA, vimentin and collagen I expression (P<0.01 at 20 µg/ml), increased the expression of E-cadherin
*Vim↓,
*COL1↓,
*E-cadherin↑,
*TGF-β1↓, and significantly downregulated the high glucose-induced expression of TGF-β1 and p-ERK1/2 in a dose-dependent manner (P<0.05).
*p‑ERK↓,
*EMT↓, suggested that high glucose concentrations induced the EMT of HK-2 cells, and that allicin was able to inhibit the EMT, potentially via regulation of the ERK1/2-TGF-β1 signaling pathway.

2696- BBR,    Berberine regulates proliferation, collagen synthesis and cytokine secretion of cardiac fibroblasts via AMPK-mTOR-p70S6K signaling pathway
- in-vivo, Nor, NA
*α-SMA↓, It was demonstrated that treatment of cardiac fibroblasts with berberine resulted in deceased proliferation, and attenuated fibroblast α-smooth muscle actin expression and collagen synthesis.
*TGF-β1↓, protein secretion of TGFβ1 was inhibited; however, the protein secretion of IL-10 was increased in cardiac fibroblasts with berberine treatment.
*IL10↑,
*p‑AMPK↑, Mechanistically, the phosphorylation level of AMPK was increased
*p‑mTOR↓, phosphorylation levels of mTOR and p70S6K were decreased in berberine treatment group
*P70S6K↓,
*cardioP↑, protective effects of berberine on cellular behaviors of cardiac fibroblasts

2694- BBR,    Berberine down-regulates IL-8 expression through inhibition of the EGFR/MEK/ERK pathway in triple-negative breast cancer cells
- in-vitro, BC, NA
IL8↓, BBR dramatically suppresses IL-8 expression.
TumCI↓, BBR also inhibited cell invasiveness
EGFR↓, BBR down-regulates EGFR protein expression and dose-dependently inhibits MEK and ERK phosphorylation.
MEK↓,
ERK↓,
TGF-β1↓, BBR inhibits the tumorigenic and angiogenic properties of TNBC cells by inhibiting TGF-β1 expression and VEGF secretion (
VEGF↓,

5988- Chit,    Chitosan immunomodulation: insights into mechanisms of action on immune cells and signaling pathways
- Review, Var, NA
DDS↑, various biomedical applications, including drug delivery, cartilage repair, wound healing, and tissue engineering, because of its unique physicochemical properties.
*Cartilage↑,
*Wound Healing↑,
Imm↑, investigation of the immunomodulatory properties of chitosan, since the biopolymer has been shown to modulate the maturation, activation, cytokine production, and polarization of dendritic cells and macrophages
cGAS–STING↑, Several signaling pathways, including the cGAS–STING, STAT-1, and NLRP3 inflammasomes, are involved in chitosan-induced immunomodulation. CS activates the cGAS–STING signaling pathway
STAT1↑, One crucial factor is DDA, as it was observed that 80% DDA CS activated the STAT-1 pathway, whereas 98% DDA did not
NLRP3↑, activation of the NLRP3 inflammasome by CS requires the presence of mitochondrial ROS.
*DCells↑, CS has been studied for its potential impact on DC activation, which is a crucial step in initiating the immune response.
*IL10↓, The use of CS also reduced IL-10 production and increased TGF-β1, TNF-α, and interleukin-1 beta (IL-1β) (p < 0.001) levels.
*TGF-β1↓,
*TNF-α↓,
IL1β↓,
ROS↑, CS internalization in DCs caused mitochondrial stress and led to the production of reactive oxygen species (ROS)

6529- CRV,    D-Carvone Attenuates CCl4-Induced Liver Fibrosis in Rats by Inhibiting Oxidative Stress and TGF-ß 1/SMAD3 Signaling Pathway
- in-vivo, Nor, NA
*ALAT↓, D-carvone significantly enhanced liver functions (ALT, AST), oxidant/antioxidant status (MDA, SOD, GSH, total antioxidant capacity; TAC), as well as histopathological changes.
*AST↓, administration with D-carvone (50 mg/kg, bw) significantly reduced serum ALT and AST to 54.8% and 51% compared to the CCl4 model group, respectively
*MDA↓, decreased the MDA levels to 50.7%, while it restored the depleted GSH and SOD levels to 233% and 221.5%, respectively
*SOD↑,
*GSH↑,
*TAC↑,
*eff↑, D-carvone effectively attenuated the progression of liver fibrosis, evident by the decreased collagen deposition and fibrosis score by Masson trichrome staining (MT) and α-SMA protein expression
*TGF-β1↓, significant downregulation of the pro-fibrogenic markers TGF-β1 and SMAD3 and upregulation of MMP9.
*SMAD3↓,
*MMP9↑,
*NRF2↑, D-carvone promotes the Nrf2 signaling pathway which might contribute to the antioxidative activity of D-carvone
*antiOx↑,
*hepatoP↑,
*Inflam↓, D-carvone administration appreciably reduced the inflammatory cells’ infiltration and pro-inflammatory modulators release provoked by liver injury
*NF-kB↓, D-carvone include downregulation of NF-κB
*NO↓, D-carvone has been reported to diminish the excessively produced NO by macrophages and Kupffer cells in the injured liver
*cAMP↑, carvone has been found to activate the cyclic adenosine monophosphate (cAMP) signaling pathway
*ROS↓, by Inhibiting Oxidative Stress

6283- DL,    D-limonene inhibits peritoneal adhesion formation in rats via anti-inflammatory, anti-angiogenic, and antioxidative effects
- in-vivo, Nor, NA
*TGF-β1↓, administration of limonene in both doses significantly reduced levels of TGF-β1, TNF-α, and VEGF (P < 0.05).
*VEGF↓,
*MDA↓, Limonene 50 group significantly reduced MDA level and increased GPx and CAT levels on day 14 (P < 0.05).
*GPx↑,
*Catalase↑,
*Inflam↓, In summary, D-limonene reduced adhesion bands, inflammatory cytokines, angiogenesis, and oxidative stress.
*ROS↓,
*angioG↓,

7012- Fuc,    Fucoidan: A promising natural therapeutic agent for protecting human kidney health
- Review, EC, NA
*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.

7046- GA,    Gallic acid: A promising anti-non-small cell lung cancer compound targeting early growth response protein-1 for apoptosis and ferroptosis
- in-vitro, NSCLC, A549 - in-vitro, NSCLC, H1299
TumCP↓, GA suppressed NSCLC cell proliferation, induced cell cycle arrest, and inhibited cell migration and invasion.
TumCCA↑,
TumCMig↓,
TumCI↓,
Apoptosis↑, GA simultaneously facilitated apoptosis and ferroptosis through EGR1 in NSCLC cells.
Ferroptosis↑,
THBS1↓, downregulating thrombospondin-1 via EGR1, inhibiting transforming growth factor beta 1/Smad2/3 signaling pathway.
EGR1↓,
TGF-β1↓,
SMAD2↓,
SMAD3↓,
GPx4↓, characterized by reduced GPX4 expression, increased reactive oxygen species and malondialdehyde accumulation, altered mitochondria, and iron overload.
ROS↑,
i-MDA↑,
i-Iron↑,

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↓,


Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   i-Iron↑, 1,   i-MDA↑, 1,   ROS↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MEK↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 2,   Apoptosis↑, 1,   Fas↓, 1,   FasL↓, 1,   Ferroptosis↑, 1,   JNK↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

TumCCA↑, 1,  

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

EMT↓, 2,   ERK↓, 1,   GSK‐3β↓, 1,   NOTCH1↓, 1,   PI3K↓, 1,   STAT1↑, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   Slug↓, 1,   Smad1↓, 1,   SMAD2↓, 1,   SMAD3↓, 1,   Snail↓, 1,   TGF-β1↓, 4,   THBS1↓, 1,   TumCI↓, 3,   TumCMig↓, 3,   TumCP↓, 2,   Vim↓, 1,   Zeb1↓, 1,   ZEB2↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

EGFR↓, 1,   EGR1↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IL1β↓, 1,   IL6↓, 1,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Cellular Microenvironment(tgid=17) ⓘ

cGAS–STING↑, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

DDS↑, 1,   Dose↝, 1,   eff↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

EGFR↓, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   chemoP↑, 1,  
Total Targets: 57

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Buty↑, 1,   diuretic↑, 1,   GLP-1R↑, 1,   SCFAs↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 2,   GPx↑, 2,   GSH↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 3,   NRF2↑, 2,   ROS↓, 3,   SOD↑, 2,   TAC↑, 1,   uricA↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1,   p‑AMPK↑, 1,   cAMP↑, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   MAPK↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

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

EMT↓, 1,   ERK↑, 1,   p‑ERK↓, 1,   p‑mTOR↓, 1,   P70S6K↓, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

Cartilage↑, 1,   COL1↓, 2,   E-cadherin↑, 1,   Fibrosis↓, 1,   MMP9↑, 1,   RAGE↓, 1,   SMAD3↓, 1,   TGF-β1↓, 6,   TJ↑, 1,   Vim↓, 1,   α-SMA↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   NO↓, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

DCells↑, 1,   HMGB1↓, 1,   IL10↓, 1,   IL10↑, 1,   Imm↑, 1,   Inflam↓, 4,   JAK2↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↝, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BloodF↑, 1,   GutMicro↑, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 1,   hepatoP↑, 1,   RenoP↑, 1,   Wound Healing↑, 1,  
Total Targets: 68

Scientific Paper Hit Count for: TGF-β1, Transforming Growth Factor-Beta 1
2 Berberine
1 Astragalus
1 Allicin (mainly Garlic)
1 chitosan
1 Carvone
1 D-limonene
1 Fucoidan
1 Gallic acid
1 Phenethyl isothiocyanate
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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