TGF-β Cancer Research Results

TGF-β, transforming growth factor-beta: Click to Expand ⟱

Source: HalifaxProj(inhibit) CGL-CS TCGA

Type:

Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses.
Anti-inflammatory cytokine.
In normal tissues, TGF-β plays an essential role in cell cycle regulation, immune function, and tissue remodeling.
- In early carcinogenesis, TGF-β typically acts as a tumor suppressor by inhibiting cell proliferation and inducing apoptosis.

In advanced cancers, cells frequently become resistant to the growth-inhibitory effects of TGF-β.
- TGF-β then switches roles and promotes tumor progression by stimulating epithelial-to-mesenchymal transition (EMT), cell invasion, metastasis, and immune evasion.

Non-canonical (Smad-independent) pathways, such as MAPK, PI3K/Akt, and Rho signaling, also contribute to TGF-β-mediated responses.

Elevated levels of TGF-β have been detected in many advanced-stage cancers, including breast, lung, colorectal, pancreatic, and prostate cancers.
- The switch from a tumor-suppressive to a tumor-promoting role is often associated with increased TGF-β production and activation in the tumor microenvironment.

High TGF-β expression or signaling activity is frequently correlated with aggressive disease features, resistance to therapy, increased metastasis, and poorer overall survival in many cancer types.

Scientific Papers found: Click to Expand⟱

4360-

AgNPs,

Silver Nanoparticles as Real Topical Bullets for Wound Healing

Study,

Nor,

*other↝, Silver therapy, in principle, has many benefits, such as (1) a multilevel antibacterial effect on cells, which considerably reduces the organism's chances of developing resistance; (2) effectiveness against multi-drug-resistant organisms;
*toxicity↓, (3) low systemic toxicity.
*eff↑, Decreasing the dimension of nanoparticles has a pronounced effect on their physical properties, which significantly differ from those of the bulk material
*eff↑, Bacterial resistance to elemental silver is extremely rare
*Inflam↓, Anti-inflammatory properties of silver nanoparticles also promote wound healing by reducing cytokine release,56 decreasing lymphocyte and mast cell infiltration.
*IL6↓, Levels of IL-6 mRNA in the wound areas treated with silver nanoparticles were maintained at statistically significantly lower levels throughout the healing process,
*TGF-β↑, mRNA levels of TGF-β1 were higher during the initial period of healing in the site treated with silver nanoparticles
*MMP9↓, Nanocrystalline silver dressings significantly reduced MMP-9 levels in a porcine mode
*eff↑, Wounds treated with silver nanoparticles completely healed in 25.2 ± 0.72 days after injury, whereas those treated with antibiotics required 28.6 ± 1.02 days (P < .01).

3667-

ART/DHA,

Artemisinin improves neurocognitive deficits associated with sepsis by activating the AMPK axis in microglia

Review,

Sepsis,

40 μΜ)

mice

*cognitive↑, artemisinin administration significantly improved LPS-induced cognitive impairments assessed in Morris water maze and Y maze tests
*neuroP↑, attenuated neuronal damage and microglial activation in the hippocampus.
*TNF-α↓, artemisinin (40 μΜ) significantly reduced the production of proinflammatory cytokines (i.e., TNF-α, IL-6)
*IL6↓,
*NF-kB↓, artemisinin significantly suppressed the nuclear translocation of NF-κB and the expression of proinflammatory cytokines by activating the AMPKα1 pathway;
*AMPK↑,
*ROS↓, artemisinin protects neuronal HT-22 cells from oxidative injury by activating the Akt pathway
*Akt↑,
*MCP1↓, artemisinin reversed the LPS-induced increases in the chemokines MCP-1 and MIP-2
*MIP2↓,
*TGF-β↑, Artemisinin also significantly increased the mRNA and protein expression of TGF-β
*Inflam↓, The AMPKα1 pathway is involved in the anti-inflammatory effect of artemisinin

5536-

BBM,

Regulation of Cell-Signaling Pathways by Berbamine in Different Cancers

Review,

Var,

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↓,

3516-

Bor,

Boron in wound healing: a comprehensive investigation of its diverse mechanisms

Review,

Wounds,

*Inflam↓, anti-inflammatory, antimicrobial, antioxidant, and pro-proliferative effects.
*antiOx↑,
*ROS↓, The antioxidant properties of boron help protect cells from oxidative stress, a common feature of chronic wounds that can impair healing
*angioG↑, Boron compounds exhibit diverse therapeutic actions in wound healing, including antimicrobial effects, inflammation modulation, oxidative stress reduction, angiogenesis induction, and anti-fibrotic properties.
*COL1↑, Boron has been shown to increase the expression of proteins involved in wound contraction and matrix remodeling, such as collagen, alpha-smooth muscle actin, and transforming growth factor-beta1.
*α-SMA↑,
*TGF-β↑,
*BMD↑, Animals treated with boron showed favorable changes in bone density, wound healing, embryonic development, and liver metabolism
*hepatoP↑,
*TNF-α↑, BA elevates TNF-α and heat-shock proteins 70 that are related to wound healing.
*HSP70/HSPA5↑,
*SOD↑, antioxidant properties of BA showed that boron protects renal tissue from I/R injury via increasing SOD, CAT, and GSH and decreasing MDA and total oxidant status (TOS)
*Catalase↑,
*GSH↑,
*MDA↓,
*TOS↓,
*IL6↓, Boron supports gastric tissue by alleviating ROS, MDA, IL-6, TNF-α, and JAK2/STAT3 action, as well as improving AMPK activity
*JAK2↓,
*STAT3↓,
*AMPK↑,
*lipid-P↓, boron may improve wound healing by hindering lipid peroxidation and increasing the level of VEGF
*VEGF↑,
*Half-Life↝, Boron is a trace element, usually found at a concentration of 0–0.2 mg/dL in plasma with a half-life of 5–10 h, and 1–2 mg of it is needed in the daily diet

1621-

EA,

The multifaceted mechanisms of ellagic acid in the treatment of tumors: State-of-the-art

Review,

Var,

AntiCan↑, Studies have shown its anti-tumor effect in gastric cancer, liver cancer, pancreatic cancer, breast cancer, colorectal cancer, lung cancer and other malignant tumors
Apoptosis↑,
TumCP↓,
TumMeta↓,
TumCI↓,
TumAuto↑,
VEGFR2↓, inhibition of VEGFR-2 signaling
MAPK↓, MAPK and PI3K/Akt pathways
PI3K↓,
Akt↓,
PD-1↓, Downregulation of VEGFR-2 and PD-1 expression
NOTCH↓, Inhibition of Akt and Notch
PCNA↓, regulation of the expression of proliferation-related proteins PCNA, Ki67, CyclinD1, CDK-2, and CDK-6
Ki-67↓,
cycD1/CCND1↓,
CDK2↑,
CDK6↓,
Bcl-2↓,
cl‑PARP↑, up-regulated the expression of cleaved PARP, Bax, Active Caspase3, DR4, and DR5
BAX↑,
Casp3↑,
DR4↑,
DR5↑,
Snail↓, down-regulated the expression of Snail, MMP-2, and MMP-9
MMP2↓,
MMP9↓,
TGF-β↑, up-regulation of TGF-β1
PKCδ↓, Inhibition of PKC signaling
β-catenin/ZEB1↓, decreases the expression level of β-catenin
SIRT1↓, down-regulates the expression of anti-apoptotic protein, SIRT1, HuR, and HO-1 protein
HO-1↓,
ROS↑, up-regulates ROS
CHOP↑, activating the CHOP signaling pathway to induce apoptosis
Cyt‑c↑, releases cytochrome c
MMP↓, decreases mitochondrial membrane potential and oxygen consumption,
OCR↓,
AMPK↑, activates AMPK, and downregulates HIF-1α expression
Hif1a↓,
NF-kB↓, inhibition of NF-κB pathway
E-cadherin↑, Upregulates E-cadherin, downregulates vimentin and then blocks EMT progression
Vim↓,
EMT↓,
LC3II↑, Up-regulation of LC3 – II expression and down-regulation of CIP2A
CIP2A↓,
GLUT1↓, regulation of glycolysis-related gene GLUT1 and downstream protein PDH expression
PDH↝,
MAD↓, Downregulation of MAD, LDH, GR, GST, and GSH-Px related protein expressio
LDH↓,
GSTs↑,
NOTCH↓, inhibited the expression of Akt and Notch protein
survivin↓, survivin and XIAP was also significantly down-regulated
XIAP↓,
ER Stress↑, through ER stress
ChemoSideEff↓, could improve cisplatin-induced hepatotoxicity in colorectal cancer cells
ChemoSen↑, Enhancing chemosensitivity

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↓,

4111-

MF,

Coupling of pulsed electromagnetic fields (PEMF) therapy to molecular grounds of the cell

Review,

Arthritis,

*Inflam↓, ultimately lead to a dampening of inflammatory signals like interleukins
*Cartilage↑, this therapy has positive effects for the regeneration of musculoskeletal tissues such as cartilage, bone, tendon and ligament
*Pain↓, Ryang We et al. [18] found a significant beneficial effect of PEMF on WOMAC pain scores at 1 month compared with a sham treatment
*QoL↑, significant improvements in mobility, daily activity score as well as global score during treatment of acute osteoarthritis of knee joint
*Dose↝, PEMF stimulation (38 Hz, 2 mT) for 2 h per day enhanced osteoblastic functions through amelioration of the cytoskeletal organization;
*VEGF↑, increase of anti-inflammatory prostaglandins, and a huge rise in the Vascular Endothelial Growth Factor (VEGF)-A-mRNA transcription.
*NO↑, stimulatory effect of PEMF on osteoblast proliferation and differentiation is accompanied by an increase in nitric oxide (NO) synthesis
*TGF-β↑, Transforming Growth Factor (TGF-β) family is enhanced by PEMF[67] and local expression of TGF-β results in improved bone fracture healing
*MMP9↓, PEMF treatment suppressed IL-1β-mediated up-regulation of MMP-9 protein levels.
*PGE2↑, Sontag and Dertinger [97] investigated the liberation of prostaglandin E2 (PGE2) during application of EMF of different frequencies: here “windows” at 6 and 16 Hz were found, where PGE was 200% above 0 Hz baseline.
*GPx3↑, PEMF exposure also induced expression of GPX3, SOD2, CAT and GSR on mRNA, protein and enzyme activity level
*SOD2↑,
*Catalase↑,
*GSR↑,
*Ca+2↑, many EMF-effect studies is a direct action on voltage-gated calcium channels (VGCCs) (Figure 1). This is normally accompanied by a rapid increase of Ca2+

3536-

MF,

Targeting Mesenchymal Stromal Cells/Pericytes (MSCs) With Pulsed Electromagnetic Field (PEMF) Has the Potential to Treat Rheumatoid Arthritis

Review,

Arthritis,

Review,

Stroke,

*Inflam↓, (PEMF), a biophysical form of stimulation, has an anti-inflammatory effect by causing differentiation of MSCs.
*Diff↑,
*toxicity∅, PEMF have been reported to last up to 3 months or longer in human patients with chronic inflammatory/autoimmune disorders (38) with no evidence of adverse effects (39).
*other↑, MSCs to promote immunomodulation and improve cartilage and bone regeneration in vitro (10) and in vivo (73).
*SOX9↑, enhanced chondrogenic gene expression in SOX-9, COL II, and aggrecan in MSCs
*COL2A1↑,
*NO↓, Prevented increases in NO
*PGE2↓, Exposure to PEMF induces early upregulation of adenosine receptors A2A and A3 that reduce PGE2 and pro-inflammatory cytokines such as TNF-α, which combine to inhibit the activation of transcription factor NF-kB
*NF-kB↓,
*TNF-α↓, 1 h exposure to PEMF has been shown to down-regulate both NF-kB and TNF-α in murine macrophages
*IL1β↓, By inhibiting NF-kB activation (94), exposure to PEMF led to decreased production of TNF-α, IL-1β, IL-6, and PGE2 in human chondrocytes, osteoblasts, and synovial fibroblasts
*IL6↓,
*IL10↑, Inhibited release of PGE2, and IL-1β and IL-6 production, while stimulating release of IL-10 in synovial fibroblasts
*angioG↑, progenitor cells (EPCs) to an RA injury site is important for repair of vasculature and angiogenesis. PEMF has also been reported to increase the number and function of circulating EPCs in treating myocardial ischemia/reperfusion (I/R) injury in rat
*MSCs↑, Since PEMF have been shown to stimulate the production of MSCs
*VEGF↑, promoting the expression of growth factors such as VEGF and TGF-β
*TGF-β↑,
*angioG↝, modulate the aberrant angiogenesis present in RA: reported to significantly reduce activation levels of VEGF (15), to inhibit the proliferative ability of HUVECs, and to reduce the extent of vascularization in diseased tissue
*VEGF↓, diseased tissue
Ca+2↝, By restoring normal Ca2+ ion flux and Na+/K+ balance, the cell can begin the process of down-regulating inflammatory cytokines, HSPs, and proangiogenic molecules such as VEGF, making it possible for the body to commence rebuilding healthy cartilage.

3468-

MF,

An integrative review of pulsed electromagnetic field therapy (PEMF) and wound healing

Review,

NA,

*other↑, studies suggest that PEMF accelerates early stages of wound closure
*necrosis↓, By preventing necrosis, PEMF can potentially be used to reduce the incidence of ulcer formation and amputation in patients with diabetes.
*IL6↑, When gingival wounds were exposed to PEMF, one study measured an increased expression of various signalling molecules involved in proliferation including IL‑6, TGF‑β and iNOS
*TGF-β↑,
*iNOS↑,
*MMP2↑, The same study also found increased levels of MMP‑2, MCP‑1 and HO‑1 expression, all of which are thought to increase wound repair rate
*MCP1↑,
*HO-1↑,
*Inflam↓, PEMF has also been shown to reduce inflammation in chronic wounds through both intracellular and extracellular effects.
*IL1β↓, Multiple studies have measured reductions in inflammatory cytokines (IL‑1β, IL‑6, TNF‑α) following PEMF treatment
*IL6↓,
*TNF-α↓,
*BioAv↑, Electrochemotherapy mediated by PEMF was found to have a 2-fold increase in drug uptake compared to traditional electrochemotherapy in rat melanoma models
eff⇅, PEMF at 50Hz, 1mT for 1 hour had increased keratinocyte proliferation compared to control groups, while the same tissue exposed to PEMF at 60Hz, 1.5mT for 144 hours had reduced cell proliferation
DNAdam↑, At higher frequencies (6–7mT), an increase in DNA double-strand breaks, apoptosis and levels of reactive oxygen species (ROS) were measured, contributing to the inhibition of cell proliferation.
Apoptosis↑,
ROS↑,
TumCP↓,
*ROS↓, tissues exposed to lower frequencies of PEMF (1mT) had decreased ROS levels
*FGF↑, Furthermore, both diabetes-related and non-diabetes-related incision wounds had similar levels of increased FGF‑2, promoting angiogenesis and preventing necrosis in response to ischaemic injury

3497-

MFrot,

MF,

The Effect of a Rotating Magnetic Field on the Regenerative Potential of Platelets

Human,

Nor,

30 healthy female and male volunteers

*PDGFR-BB↑, The highest concentration of PDGF-BB was observed in the samples placed in RMF for 1 h at 25 Hz
*TGF-β↑, For TGF-β1, the highest concentrations were obtained in the samples exposed to RMF for 3 h at 25 Hz and 1 h at 50 Hz.
*IGF-1↑, highest concentrations of IGF-1 and FGF-1 were shown in plasma placed in RMF for 3 h at 25 Hz.
*FGF↑,
*angioG↑, Magnetic fields have been shown to have a beneficial effect on vasodilation, angiogenesis, accelerating repair, regeneration, and healing of soft tissues, nervous tissues and bones, analgesic aspects, anti-swelling, reducing inflammation and pain, an
*Inflam↓,
*ROS↓, RMF exposure can increase resistance to heat stress, reduce levels of ROS, affect intracellular calcium ion concentrations, and contribute to cell aging deceleration

2048-

PB,

Sodium Phenylbutyrate Inhibits Tumor Growth and the Epithelial-Mesenchymal Transition of Oral Squamous Cell Carcinoma In Vitro and In Vivo

in-vitro,

OS,

CAL27

4mM

in-vitro,

Oral,

HSC3

3.7mM

in-vitro,

OS,

SCC4

3mM

in-vivo,

NA,

*NH3↓, Sodium phenylbutyrate (SPB) as a salt of 4-phenylbutyric acid (4-PBA) has been reported to be an ammonia scavenger, histone deacetylase inhibitor, and an endoplasmic reticulum stress inhibitor
*HDAC↓,
*ER Stress↓,
Apoptosis?, SPB could significantly promote cell apoptosis
Bcl-2↓, BCL-2 was downregulated
cl‑Casp3↑, cleavage of caspase-3 was increased
TGF-β↑, transforming growth factor-β (TGFB) related epithelial-mesenchymal transition (EMT) was inhibited by SPB
N-cadherin↓, decreased mesenchymal marker N-cadherin and increased epithelial marker E-cadherin.
E-cadherin↑,
TumVol↓, SPB induced remarkably tumor regression with decreased tumor volume
eff↑, phenylbutyrate improved the sensitivity of cisplatin for cell cycle arrest by inhibiting the FA/BRCA pathway in cancer cells.

1681-

PBG,

Propolis: Its Role and Efficacy in Human Health and Diseases

Review,

Nor,

*Inflam↓,
*AntiCan↑,
*antiOx↑,
*hyperG↓, flavanone glycoside found in propolis, has been reported to have insulin-like and lipid-reducing properties that reduce both insulin resistance and hyperglycemia
*BG↓, These flavonoids, including apigenin, naringin, chrysin, galangin, kaempferol, luteolin, genistein, and quercetin help to reduce blood glucose concentration
*HbA1c↓, propolis showed significant effects, reducing the blood glucose levels, serum insulin, and serum glycosylated haemoglobin (HbA1c) levels of T2DM patients
*NF-kB↓, propolis can also suppress inflammatory cascades by blocking the NF-κB pathway and reducing ROS by enhancing antioxidants
*ROS↓,
*TGF-β↑, formation of the transforming growth factor-β1 (TGF-β1) of the cells are promoted by the caffeic acid, CAPE, hesperidin, and quercetin of propolis
*selectivity↑, CAPE is a very significant compound of propolis that has anti-inflammatory properties and also acts as the selective inhibitor of NF-κB activation

2213-

SK,

Shikonin attenuates cerebral ischemia/reperfusion injury via inhibiting NOD2/RIP2/NF-κB-mediated microglia polarization and neuroinflammation

in-vivo,

Stroke,

 MCAO/R rats

*neuroP↑, Shikonin treatment significantly reduced brain infarction volume and improved neurological function in MCAO/R rats.
*Inflam↓, Shikonin treatment significantly reduced microglial proinflammatory phenotype and levels of proinflammatory markers (inducible-NO synthase (iNOS), tumor necrosis factor-alpha (TNF-α),
*iNOS↓,
*TNF-α↓,
*IL1β↓, interleukin-1 beta (IL-1β), and IL-6), increased microglial anti-inflammatory phenotype and levels of anti-inflammatory markers (Arginase-1 (Arg1), transforming growth factor-beta (TGF-β), and IL-10),
*IL6↓,
*ARG↑,
*TGF-β↑,
*IL10↑,
*NF-kB↓, reversed the expression of Nucleotide-binding oligomerization domain 2 (NOD2) and phosphorylation receptor interacting protein 2 (p-RIP2), and suppressed nuclear factor kappa-B (NF-κB) signaling activation in the ischemic penumbra regions.
*eff↓, Furthermore, overexpression of NOD2 markedly attenuated the neuroprotective effects of Shikonin treatment in MCAO/R rats.

3425-

TQ,

Advances in research on the relationship between thymoquinone and pancreatic cancer

Apoptosis↑, TQ can inhibit cell proliferation, promote cancer cell apoptosis, inhibit cell invasion and metastasis, enhance chemotherapeutic sensitivity, inhibit angiogenesis, and exert anti-inflammatory effects.
TumCP↓,
TumCI↓,
TumMeta↓,
ChemoSen↑,
angioG↓,
Inflam↓,
NF-kB↓, These anticancer effects predominantly involve the nuclear factor (NF)-κB, phosphoinositide 3 kinase (PI3K)/Akt, Notch, transforming growth factor (TGF)-β, c-Jun N-terminal kinase (JNK)
PI3K↓,
Akt↓,
TGF-β↓,
Jun↓,
p38↑, and p38 mitogen-activated protein kinase (MAPK) signaling pathways as well as the regulation of the cell cycle, matrix metallopeptidase (MMP)-9 expression, and pyruvate kinase isozyme type M2 (PKM2) activity.
MAPK↑, activation of the JNK and p38 MAPK
MMP9↓,
PKM2↓, decrease in PKM2 activity
ROS↑, ROS-mediated activation
JNK↑, activation of the JNK and p38 MAPK
MUC4↓, downregulation of MUC4;
TGF-β↑, TQ led to the activation of the TGF-β pathway and subsequent downregulation of MUC4
Dose↝, Q acts as an antioxidant (free radical scavenger) at low concentrations and as a pro-oxidant at high concentrations.
FAK↓, TQ can inhibit several key molecules such as FAK, Akt, NF-κB, and MMP-9 and that these molecules interact in a cascade to affect the metastasis of pancreatic cancer
NOTCH↓, TQ involved in increasing chemosensitivity consist of blocking the Notch1/PTEN, PI3K/Akt/mTOR, and NF-κB signaling pathways, reducing PKM2 expression, and inhibiting the Warburg effect.
PTEN↑, it also restored the PTEN protein that had been inhibited by GEM
mTOR↓,
Warburg↓, reducing PKM2 expression, and inhibiting the Warburg effect.
XIAP↓,
COX2↓,
Casp9↑,
Ki-67↓,
CD34↓,
VEGF↓,
MCP1↓,
survivin↓,
Cyt‑c↑,
Casp3↑,
H4↑,
HDAC↓,

1223-

VitD3,

Vitamin D3 Treatment Influences PGE2 and TGFβ in Normal and Increased Breast Cancer Risk Women

Trial,

NA,

 We reported that vitamin D3 increased transforming growth factor (TGF)β2 and decreased prostaglandin (PG)E2 in the breast of normal-risk women, suggesting a protective effect.

*TGF-β↑, TGFβ2 increase correlated with increase in 25(OH)D. DBP serum levels
*PGE2↓,

Showing Research Papers: 1 to 15 of 15

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 2, Catalase↑, 2, GPx3↑, 1, GSH↑, 1, GSR↑, 1, HO-1↑, 1, hyperG↓, 1, lipid-P↓, 1, MDA↓, 1, ROS↓, 5, SOD↑, 1, SOD2↑, 1, TOS↓, 1,

Core Metabolism/Glycolysis ⓘ

AMPK↑, 2, NH3↓, 1,

Cell Death ⓘ

Akt↑, 1, iNOS↓, 1, iNOS↑, 1, necrosis↓, 1,

Kinase & Signal Transduction ⓘ

SOX9↑, 1,

Transcription & Epigenetics ⓘ

other↑, 2, other↝, 1,

Protein Folding & ER Stress ⓘ

ER Stress↓, 1, HSP70/HSPA5↑, 1,

Proliferation, Differentiation & Cell State ⓘ

Diff↑, 1, FGF↑, 2, HDAC↓, 1, IGF-1↑, 1, MSCs↑, 1, STAT3↓, 1,

Migration ⓘ

ARG↑, 1, Ca+2↑, 1, Cartilage↑, 1, COL1↑, 1, COL2A1↑, 1, MMP2↑, 1, MMP9↓, 2, TGF-β↑, 10, α-SMA↑, 1,

Angiogenesis & Vasculature ⓘ

angioG↑, 3, angioG↝, 1, NO↓, 1, NO↑, 1, PDGFR-BB↑, 1, VEGF↓, 1, VEGF↑, 3,

Immune & Inflammatory Signaling ⓘ

IL10↑, 2, IL1β↓, 3, IL6↓, 6, IL6↑, 1, Inflam↓, 9, JAK2↓, 1, MCP1↓, 1, MCP1↑, 1, MIP2↓, 1, NF-kB↓, 4, PGE2↓, 2, PGE2↑, 1, TNF-α↓, 4, TNF-α↑, 1,

Drug Metabolism & Resistance ⓘ

BioAv↑, 1, Dose↝, 1, eff↓, 1, eff↑, 3, Half-Life↝, 1, selectivity↑, 1,

Clinical Biomarkers ⓘ

BG↓, 1, BMD↑, 1, HbA1c↓, 1, IL6↓, 6, IL6↑, 1,

Functional Outcomes ⓘ

AntiCan↑, 1, cognitive↑, 1, hepatoP↑, 1, neuroP↑, 2, Pain↓, 1, QoL↑, 1, toxicity↓, 1, toxicity∅, 1,
Total Targets: 79

Scientific Paper Hit Count for: TGF-β, transforming growth factor-beta

4 Magnetic Fields
1 Silver-NanoParticles
1 Artemisinin
1 Berbamine
1 Boron
1 Ellagic acid
1 Emodin
1 Magnetic Field Rotating
1 Phenylbutyrate
1 Propolis -bee glue
1 Shikonin
1 Thymoquinone
1 Vitamin D3

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#:304  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

TGF-β 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 ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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