β-catenin/ZEB1 Cancer Research Results

β-catenin/ZEB1, β-catenin/ZEB1: Click to Expand ⟱

Source: HalifaxProj (inactivate)

Type:

β-catenin and ZEB1 are two important proteins that play significant roles in cancer biology, particularly in the processes of cell adhesion, epithelial-mesenchymal transition (EMT), and tumor progression.
β-catenin is a key component of the Wnt signaling pathway, which is crucial for cell proliferation, differentiation, and survival. It also plays a role in cell-cell adhesion by linking cadherins to the actin cytoskeleton.
Role in Cancer: ZEB1 is often upregulated in cancer and is associated with increased invasiveness and metastasis. It can repress epithelial markers (like E-cadherin) and promote mesenchymal markers (like N-cadherin and vimentin), facilitating the transition to a more aggressive cancer phenotype.

(MMP)-2 and MMP-9, which are the down-stream targets of β-catenin and play a crucial role in cancer cell metastasis.

Scientific Papers found: Click to Expand⟱

3521-

Bor,

A new hope for obesity management: Boron inhibits adipogenesis in progenitor cells through the Wnt/β-catenin pathway

in-vitro,

Obesity,

3T3

*CEBPA↓, Figure 2
*PPARγ↓,
*FASN↓,
*SREBP1↓,
*FABP4↓,
*GLUT4↓,
*β-catenin/ZEB1↑, Boron Activated the Î²-Catenin Signaling Pathway
*MMP2↓, As shown in Fig. 6, soluble transforming growth factor receptor 1 (sTNFR1) and matrix metalloproteinase 2 (MMP2) protein levels decreased in the presence of boron
*FGF↑, whereas basic fibroblast growth factor expression (bFGF) increased
*Ca+2?, Boric acid has been reported to interact with NAD + and inhibit cyclic ADP ribose-activated Ca 2+ release from ryanodine receptor, leading to decreased endoplasmic reticulum luminal Ca 2+ concentrations

4270-

Bos,

Boswellic acids ameliorate neurodegeneration induced by AlCl3: the implication of Wnt/β-catenin pathway

in-vivo,

AD,

 6 weeks, rats were treated daily with AlCl3

*memory↑, BA significantly improved learning and memory impairments induced by AlCl3 treatment.
*AChE↓, BA treatment significantly decreased acetylcholinesterase levels and reduced amyloid-beta (Aβ) expression
*Aβ↓,
*TNF-α↓, BA ameliorated the increased expression of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β), inhibited lipid peroxidation, and increased total antioxidants in the brain.
*IL1β↓,
*lipid-P↓,
*TAC↑,
*BDNF↑, Indeed, BA significantly suppressed AlCl3-induced decrease of brain-derived neurotrophic factor, pGSK-3β (Ser 9), and β-catenin.
*β-catenin/ZEB1↑,
*Dose↑, BA (250 mg/kg) showed a significant protective effect compared to a lower dose.

6040-

CGA,

Protective effect of chlorogenic acid on cognitive impairment in rats with early Alzheimer's disease via Wnt signaling pathway

in-vivo,

AD,

Forty male rats

*neuroP↑, Chlorogenic acid (CGA) has neuroprotective properties associated with Alzheimer's disease (AD).
*Dose↝, gavage of CGA at a dose of 150 mg/kg/d
*GSK‐3β↓, decreased the expression of inflammatory factors, decreased the expression levels of GSK-3β, GFAP, and tau, and increased the expression levels of DVL2 and β-catenin.
*tau↓,
*β-catenin/ZEB1↑,
*Wnt↑, CGA can protect the cognitive impairment of early AD rats via Wnt signaling pathway. we hypothesized that activation of the Wnt signaling pathway can improve cognitive dysfunction in AD rats.
*memory↑, The results showed that CGA could improve the learning and memory ability and cognitive impairment of AD rats via Wnt signaling pathway
*cognitive↑, The result indicated that the CGA group could effectively improve the learning, memory and cognitive impairment of AD rats
*NRF2↑, CGA had a neuroprotective effect on the CI/R rats by regulating the oxidative stress-related Nrf2 pathway.
*ROS↓,

165-

CUR,

Curcumin interrupts the interaction between the androgen receptor and Wnt/β-catenin signaling pathway in LNCaP prostate cancer cells

in-vitro,

Pca,

LNCaP

AR↓, Curcumin was shown to induce significant inhibition of AR expression in a dose-dependent manner
β-catenin/ZEB1↓, Curcumin repressed the nuclear accumulation of b-catenin
p‑Akt↓, In this study, we showed that curcumin suppressed phosphorylation of both Akt and GSK-3b.
GSK‐3β↓,
p‑β-catenin/ZEB1↑, phosphorylated
cycD1/CCND1↓, cyclin D1 and c-myc, the target gene of the β-catenin/T-cell factor transcriptional complex, were also decreased
cMyc↓,
chemoPv↑, Curcumin, a dietary yellow pigment of Curcuma longa, has emerged as having a chemopreventive role.
TumCP↓, Curcumin inhibited the proliferation of LNCaP prostate cancer cells

4659-

HNK,

Honokiol Eliminates Human Oral Cancer Stem-Like Cells Accompanied with Suppression of Wnt/β-Catenin Signaling and Apoptosis Induction

in-vitro,

Oral,

cl‑Casp3↑, Apoptosis of honokiol-treated SP cells was evidenced by increased annexin V staining and cleaved caspase-3 as well as decreased Survivin and Bcl-2.
survivin↓,
Bcl-2↓,
CD44↓, Mechanistically, honokiol inhibited the CD44 and Wnt/β-catenin signaling of SP cells
Wnt↓,
β-catenin/ZEB1↑,
EMT↓, EMT markers such as Slug and Snail were markedly suppressed by honokiol.
Slug↓,
Snail↓,
CSCs↓, Our findings indicate honokiol may be able to eliminate oral cancer stem cells through apoptosis induction, suppression of Wnt/β-catenin signaling, and inhibition of EMT.
Apoptosis↑, Honokiol-Induced Apoptosis of SAS SP Cells

2869-

HNK,

Nature's neuroprotector: Honokiol and its promise for Alzheimer's and Parkinson's

Review,

AD,

Review,

Park,

*neuroP↑, neuroprotective, anti-oxidant, anti-apoptotic, neuromodulating, anti-inflammatory, and many more qualities, honokiol,
*Inflam↓,
*motorD↑, degradation of dopaminergic neurons in Parkinson's disease and improving motor function.
*Aβ↓, Alzheimer's disease, honokiol showed promise in lowering the production of amyloid-beta (Aβ) plaques, phosphorylating tau, and enhancing cognitive performance
*p‑tau↓,
*cognitive↑,
*memory↑, prevented Acetylcholinesterase activity from elevation as well as improved acetylcholine levels, and improved learning, and memory deficits via increased ERK1/2 and Akt phosphorylation
*ERK↑,
*p‑Akt↑,
*PPARγ↑, honokiol has been reported to elevate PPARγ levels in APPswe/PS1dE9 mice as PPARγ is related to ani-inflammatory
*PGC-1α↑, honokiol boosted the expression of PGC1α and PPARγ
*MMP↑, as well as reduced elevated mitochondrial membrane potential and mitochondrial ROS
*mt-ROS↓,
*SIRT3↑, Honokiol has been found as a dual SIRT-3 activator and PPAR-γ agonist that reduced oxidative stress markers within cells and changed the AMPK pathway
*IL1β↓, honokiol prevented restraint stress-induced cognitive dysfunction by reducing the hippocampus's production of IL-1β, TNF-α, glucose-regulated protein (GRP78), and C/EBP homologous protein (CHOP)
*TNF-α↓,
*GRP78/BiP↓,
*CHOP↓,
*NF-kB↓, Additionally, the neuroprotective benefits of honokiol in mice with Aβ-induced learning and memory impairment have been attributed to the inactivation of NF-κB
*GSK‐3β↓, Treatment of honokiol in PC12 cells resulted in reduced GSK-3β and induced β-catenin which effectively showed the neuroprotective and anti-oxidant effect in AD therapy
*β-catenin/ZEB1↑,
*Ca+2↓, , anti-apoptotic effect via reduced caspase 3 levels, and protected membrane injury by reduced calcium level has been investigated in PC12 cells of AD models
*AChE↓, protective effects by serving as an antioxidant, reduced AchE levels, repaired neurofibrillary tangles, reduced NF-kB which downregulates Aβ plaque
*SOD↑, fig1
*Catalase↑,
*GPx↑,

2864-

HNK,

Honokiol: A Review of Its Anticancer Potential and Mechanisms

Review,

Var,

TumCCA↑, induction of G0/G1 and G2/M cell cycle arrest
CDK2↓, (via the regulation of cyclin-dependent kinase (CDK) and cyclin proteins),
EMT↓, epithelial–mesenchymal transition inhibition via the downregulation of mesenchymal markers
MMPs↓, honokiol possesses the capability to supress cell migration and invasion via the downregulation of several matrix-metalloproteinases
AMPK↑, (activation of 5′ AMP-activated protein kinase (AMPK) and KISS1/KISS1R signalling)
TumCI↓, inhibiting cell migration, invasion, and metastasis, as well as inducing anti-angiogenesis activity (via the down-regulation of vascular endothelial growth factor (VEGFR) and vascular endothelial growth factor (VEGF)
TumCMig↓,
TumMeta↓,
VEGFR2↓,
*antiOx↑, diverse biological activities, including anti-arrhythmic, anti-inflammatory, anti-oxidative, anti-depressant, anti-thrombocytic, and anxiolytic activities
*Inflam↓,
*BBB↑, Due to its ability to cross the blood–brain barrier
*neuroP↑, beneficial towards neuronal protection through various mechanism, such as the preservation of Na+/K+ ATPase, phosphorylation of pro-survival factors, preservation of mitochondria, prevention of glucose, reactive oxgen species (ROS), and inflammatory
*ROS↓,
Dose↝, Generally, the concentrations used for the in vitro studies are between 0–150 μM
selectivity↑, Interestingly, honokiol has been shown to exhibit minimal cytotoxicity against on normal cell lines, including human fibroblast FB-1, FB-2, Hs68, and NIH-3T3 cells
Casp3↑, ↑ Caspase-3 & caspase-9
Casp9↑,
NOTCH1↓, Inhibition of Notch signalling: ↓ Notch1 & Jagged-1;
cycD1/CCND1↓, ↓ cyclin D1 & c-Myc;
cMyc↓,
P21?, ↑ p21WAF1 protein
DR5↑, ↑ DR5 & cleaved PARP
cl‑PARP↑,
P53↑, ↑ phosphorylated p53 & p53
Mcl-1↑, ↓ Mcl-1 protein
p65↓, ↓ p65; ↓ NF-κB
NF-kB↓,
ROS↑, ↑ JNK activation ,Increase ROS activity:
JNK↑,
NRF2↑, ↑ Nrf2 & c-Jun protein activation
cJun↑,
EF-1α↓, ↓ EFGR; ↓ MAPK/PI3K pathway activity
MAPK↓,
PI3K↓,
mTORC1↓, ↓ mTORC1 function; ↑ LKB1 & cytosolic localisation
CSCs↓, Inhibit stem-like characteristics: ↓ Oct4, Nanog & Sox4 protein; ↓ STAT3;
OCT4↓,
Nanog↓,
SOX4↓,
STAT3↓,
CDK4↓, ↓ Cdk2, Cdk4 & p-pRbSer780;
p‑RB1↓,
PGE2↓, ↓ PGE2 production ↓ COX-2 ↑ β-catenin
COX2↓,
β-catenin/ZEB1↑,
IKKα↓, ↓ IKKα
HDAC↓, ↓ class I HDAC proteins; ↓ HDAC activity;
HATs↑, ↑ histone acetyltransferase (HAT) activity; ↑ histone H3 & H4
H3↑,
H4↑,
LC3II↑, ↑ LC3-II
c-Raf↓, ↓ c-RAF
SIRT3↑, ↑ Sirt3 mRNA & protein; ↓ Hif-1α protein
Hif1a↓,
ER Stress↑, ↑ ER stress signalling pathway activation; ↑ GRP78,
GRP78/BiP↑,
cl‑CHOP↑, ↑ cleaved caspase-9 & CHOP;
MMP↓, mitochondrial depolarization
PCNA↓, ↓ cyclin B1, cyclin D1, cyclin D2 & PCNA;
Zeb1↓, ↓ ZEB2 Inhibit
NOTCH3↓, ↓ Notch3/Hes1 pathway
CD133↓, ↓ CD133 & Nestin protein
Nestin↓,
ATG5↑, ↑ Atg7 protein activation; ↑ Atg5;
ATG7↑,
survivin↓, ↓ Mcl-1 & survivin protein
ChemoSen↑, honokiol potentiated the apoptotic effect of both doxorubicin and paclitaxel against human liver cancer HepG2 cells.
SOX2↓, Honokiol was shown to downregulate the expression of Oct4, Nanog, and Sox2 which were known to be expressed in osteosarcoma, breast carcinoma and germ cell tumours
OS↑, Lipo-HNK was also shown to prolong survival and induce intra-tumoral apoptosis in vivo.
P-gp↓, Honokiol was shown to downregulate the expression of P-gp at mRNA and protein levels in MCF-7/ADR, a human breast MDR cancer cell line
Half-Life↓, For i.v. administration, it has been found that there was a rapid rate of distribution followed by a slower rate of elimination (elimination half-life t1/2 = 49.22 min and 56.2 min for 5 mg or 10 mg of honokiol, respectively
Half-Life↝, male and female dogs was assessed. The elimination half-life (t1/2 in hours) was found to be 20.13 (female), 9.27 (female), 7.06 (male), 4.70 (male), and 1.89 (male) after administration of doses of 8.8, 19.8, 3.9, 44.4, and 66.7 mg/kg, respectively.
eff↑, Apart from that, epigallocatechin-3-gallate functionalized chitin loaded with honokiol nanoparticles (CE-HK NP), developed by Tang et al. [224], inhibit HepG2
BioAv↓, extensive biotransformation of honokiol may contribute to its low bioavailability.

4535-

MAG,

5-FU,

Magnolol and 5-fluorouracil synergy inhibition of metastasis of cervical cancer cells by targeting PI3K/AKT/mTOR and EMT pathways

in-vitro,

Cerv,

ChemoSen↑, this study suggests that 5-FU combined with magnolol exerts a synergistic anti-cervical cancer effect by regulating the PI3K/AKT/mTOR and epithelial-mesenchymal transition (EMT) signaling pathways.
TumCP↓, magnolol strongly inhibited cervical cancer cell proliferation,
vinculin↓, down-regulating the expression of α-actinin, tensin-2 and vinculin
TumCA↓, magnolol enhanced inhibitory effect of 5-FU on the cell adhesion, migration and invasion.
TumCMig↓,
TumCI↓,
p‑Akt↓, phosphorylation of AKT and PI3K and the expression of mTOR were strongly inhibited by the combination of 5-FU and magnolol.
p‑PI3K↓,
mTOR↓,
E-cadherin↑, expression of E-cadherin and β-catenin was upregulated
β-catenin/ZEB1↑,
Snail↓, expression of Snail, Slug and vimentin was down-regulated by the 5-FU together with magnolol.
Slug↓,

2240-

MF,

Pulsed electromagnetic field induces Ca2+-dependent osteoblastogenesis in C3H10T1/2 mesenchymal cells through the Wnt-Ca2+/Wnt-β-catenin signaling pathway

in-vitro,

Nor,

C3H10T1/2

30 Hz, 1 mT, 2 h/day

PEMF output waveform consisted of a 400 kV/m pulsed burst (pulse width 0.2 m s; pulse wait 0.02 m s; burst width 5 m s; burst wait 60 m s; pulse rise 0.3 m s; pulse fall 2.0 m s) repeated at 30 Hz.

*Ca+2↑, intracellular [Ca2+]i in C3H10T1/2 cells can be upregulated upon exposure to PEMF
*Diff↑, PEMF-induced C3H10T1/2 cell differentiation was Ca2+-dependent.
*BMD↑, pro-osteogenic effect of PEMF on Ca2+-dependent osteoblast differentiation
*Wnt↑, PEMF promoted the gene expression and protein synthesis of the Wnt/β-catenin pathway.
*β-catenin/ZEB1↑, PEMF activates the Wnt/b-catenin signaling pathway in C3H10T1/2 cells
*eff↝, These data indicated that increased intranuclear [Ca2+]i resulted in altered electrical activity in the nucleus.

3477-

MF,

Electromagnetic fields regulate calcium-mediated cell fate of stem cells: osteogenesis, chondrogenesis and apoptosis

Review,

NA,

*Ca+2↑, When cells are subjected to external mechanical stimulation, voltage-gated ion channels in the cell membrane open and intracellular calcium ion concentration rises
*VEGF↑, BMSCs EMF combined with VEGF promote osteogenesis and angiogenesis
*angioG↑,
Ca+2↑, 1 Hz/100 mT MC4-L2 breast cancer cells EMF lead to calcium ion overload and ROS increased, resulting in necroptosis
ROS↑,
Necroptosis↑,
TumCCA↑, 50 Hz/4.5 mT 786-O cells ELF-EMF induce G0/G1 arrest and apoptosis in cells lines
Apoptosis↑,
*ATP↑, causing the ATP or ADP increases, and the purinergic signal can upregulate the expression of P2Y1 receptors
*FAK↑, Our research team [53] found that ELE-EMF can induce calcium oscillations in bone marrow stem cells, up-regulated calcium ion activates FAK pathway, cytoskeleton enhancement, and migration ability of stem cells in vitro is enhanced.
*Wnt↑, ability of EMF to activate the Wnt10b/β-catenin signaling pathway to promote osteogenic differentiation of cells depends on the functional integrity of primary cilia in osteoblasts.
*β-catenin/ZEB1↑,
*ROS↑, we hypothesize that the electromagnetic field-mediated calcium ion oscillations, which causes a small amount of ROS production in mitochondria, regulates the chondrogenic differentiation of cells, but further studies are needed
p38↑, RF-EMF was able to suppress tumor stem cells by activating the CAMKII/p38 MAPK signaling pathway after inducing calcium ion oscillation and by inhibiting the β-catenin/HMGA2 signaling pathway
MAPK↑,
β-catenin/ZEB1↓,
CSCs↓, Interestingly, the effect of electromagnetic fields is not limited to tumor stem cells, but also inhibits the proliferation and development of tumor cells
TumCP↓,
ROS↑, breast cancer cell lines exposed to ELE-EMF for 24 h showed a significant increase in intracellular ROS expression and an increased sensitivity to further radiotherapy
RadioS↑,
Ca+2↑, after exposure to higher intensity EMF radiation, showed a significant increase in intracellular calcium ion and reactive oxygen species, which eventually led to necroptosis
eff↓, while this programmed necrosis of tumor cells was able to be antagonized by the calcium blocker verapamil or the free radical scavenger n -acetylcysteine
NO↑, EMF can regulate multiple ions in cells, and calcium ion play a key role [92, 130], calcium ion acts as a second messenger that can activate downstream molecules such as NO, ROS

530-

MF,

Low frequency sinusoidal electromagnetic fields promote the osteogenic differentiation of rat bone marrow mesenchymal stem cells by modulating miR-34b-5p/STAC2

in-vivo,

Nor,

15 Hz, 0.4 -1 mT

rat bone marrow mesenchymal stem cells

*miR-34b-5p↓, expression of miR-34b-5p decreased under SEMF stimulation,
*ALP↑, significant upregulation in the relative expression levels of osteogenic markers (ALP, RUNX2, BMP2, OCN, and OPN)
*RUNX2↑,
*BMP2↑,
*OCN↑,
*OPN↑,
*β-catenin/ZEB1↑, protein expression levels of osteogenic makers, including Active-β-catenin, RUNX2, and ALP, were elevated upon SEMFs exposure at 0.4 mT, 0.7 mT, and 1 mT
*STAC2↑, subsequently increasing STAC2 level.
*Diff↑, electromagnetic fields promote the osteogenic differentiation
*BMD↑, low-frequency SEMFs promote osteogenesis

3745-

MFrot,

MF,

The neurobiological foundation of effective repetitive transcranial magnetic brain stimulation in Alzheimer's disease

Review,

AD,

*neuroP↑, neuroprotective actions aimed at mitigatingoxidative stress and inflammation, and intense stimulation of neu-rotrophic factors
*ROS↓,
*Inflam↓,
*5HT↑, increase in serotoninand its metabolites and a change in the properties of serotonergicreceptors.
*cFos↑, in rats, a single session of bothLF- (1 Hz) and HF-rTMS (10 Hz) enhanced c-Fos expression in all exam-ined cortical areas
*Aβ↓, rTMS enhances neuronal viability and counteracts oxidative stressors, such as Aβ and glutamate toxicity, in vitro
*memory↑, downregulation results in memory impairments
*BDNF↑, long-term change in synaptic proteinexpression due to BDNF-TrkB pathway activation following rTMSprotocols
*Ach↑, rTMSincreases ACh levels by modulating AChE activity.
*AChE↓,
*cognitive↑, HF-rTMS (20 Hz) and LF-rTMS (1 Hz)—in termsof neurotransmitter circuits and neurogenic signaling. 142 While bothprotocols improved cognition-related behaviors
*BDNF↑, Notably, rTMS could enhance BDNF and NGF expression irrespec-tive of frequency,
*NGF↑,
*β-catenin/ZEB1↑, both LF-rTMS (1 Hz) and HF-rTMS (10 Hz)protocols enhanced cognitive performance through the activation of β-catenin via the regulation of glycogen synthase kinase-3β (GSK-3β) andTau
*p‑Akt↓, 3 weeks, iTBS reducedinflammation and increased anti-inflammatory molecules, specificallylinked to reversing the downregulation of phosphorylated forms ofAkt and the mammalian target of rapamycin.
*mTOR↓,
*MMP1↓, 6 months, patients showed significant reductions in plasma levels of MMP1, MMP9, and MMP10, along with increases in TIMP1 and TIMP2
*MMP9↓,
*MMP-10↓,
*TIMP1↑,
*TIMP2↑,

1807-

NarG,

A Systematic Review of the Preventive and Therapeutic Effects of Naringin Against Human Malignancies

Review,

NA,

AntiTum↑, antitumor ability of naringin
TumCP↓,
tumCV↓,
TumCCA↑,
Mcl-1↓,
RAS↓,
e-Raf↓, suppressing the Ras/Raf/extracellular
VEGF↓,
AntiAg↑,
MMP2↓,
MMP9↓,
TIMP2↑,
TIMP1↑,
p38↓,
Wnt↓,
β-catenin/ZEB1↑,
Casp↑,
P53↑,
BAX↑,
COX2↓,
GLO-I↓,
CYP1A1↑,
lipid-P↓,
p‑Akt↓,
p‑mTOR↓,
VCAM-1↓,
P-gp↓,
survivin↓,
Bcl-2↓,
ROS↑, ↑oxidative stress, Prostate DU145 cell line 50–250 μM
ROS↑, ↑ROS, Stomach (Gastric) AGS cell line, 1–3 mM
MAPK↑,
STAT3↓,
chemoP↑, flavonoids have excellent radical scavenging and iron-chelating properties (Kaiserová et al., 2007), and they can act as an effective modulator for DOX-induced toxicity

Showing Research Papers: 1 to 13 of 13

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 13

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 1, GPx↑, 1, lipid-P↓, 1, NRF2↑, 1, ROS↓, 3, ROS↑, 1, mt-ROS↓, 1, SIRT3↑, 1, SOD↑, 1, TAC↑, 1,

Mitochondria & Bioenergetics ⓘ

ATP↑, 1, MMP↑, 1, PGC-1α↑, 1,

Core Metabolism/Glycolysis ⓘ

FABP4↓, 1, FASN↓, 1, PPARγ↓, 1, PPARγ↑, 1, SREBP1↓, 1,

Cell Death ⓘ

p‑Akt↓, 1, p‑Akt↑, 1, BMP2↑, 1,

Kinase & Signal Transduction ⓘ

OCN↑, 1,

Transcription & Epigenetics ⓘ

Ach↑, 1,

Protein Folding & ER Stress ⓘ

CHOP↓, 1, GRP78/BiP↓, 1,

Proliferation, Differentiation & Cell State ⓘ

CEBPA↓, 1, cFos↑, 1, Diff↑, 2, ERK↑, 1, FGF↑, 1, GSK‐3β↓, 2, mTOR↓, 1, RUNX2↑, 1, Wnt↑, 3,

Migration ⓘ

Ca+2?, 1, Ca+2↓, 1, Ca+2↑, 2, FAK↑, 1, MMP-10↓, 1, MMP1↓, 1, MMP2↓, 1, MMP9↓, 1, OPN↑, 1, STAC2↑, 1, TIMP1↑, 1, TIMP2↑, 1, β-catenin/ZEB1↑, 8,

Angiogenesis & Vasculature ⓘ

angioG↑, 1, miR-34b-5p↓, 1, VEGF↑, 1,

Barriers & Transport ⓘ

BBB↑, 1, GLUT4↓, 1,

Immune & Inflammatory Signaling ⓘ

IL1β↓, 2, Inflam↓, 3, NF-kB↓, 1, TNF-α↓, 2,

Synaptic & Neurotransmission ⓘ

5HT↑, 1, AChE↓, 3, BDNF↑, 3, NGF↑, 1, tau↓, 1, p‑tau↓, 1,

Protein Aggregation ⓘ

Aβ↓, 3,

Drug Metabolism & Resistance ⓘ

Dose↑, 1, Dose↝, 1, eff↝, 1,

Clinical Biomarkers ⓘ

ALP↑, 1, BMD↑, 2,

Functional Outcomes ⓘ

cognitive↑, 3, memory↑, 4, motorD↑, 1, neuroP↑, 4,
Total Targets: 73

Scientific Paper Hit Count for: β-catenin/ZEB1, β-catenin/ZEB1

4 Magnetic Fields
3 Honokiol
1 Boron
1 Boswellia (frankincense)
1 Chlorogenic acid
1 Curcumin
1 Magnolol
1 5-fluorouracil
1 Magnetic Field Rotating
1 Naringin

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

β-catenin/ZEB1 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 ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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