Wnt Cancer Research Results

Wnt, Wingless-related integration site: Click to Expand ⟱
Source:
Type:
The Wnt signaling pathway is a complex network of proteins that plays a crucial role in various cellular processes, including cell proliferation, differentiation, and migration. It is particularly important during embryonic development and tissue homeostasis. Dysregulation of the Wnt pathway has been implicated in various cancers, making it a significant area of research in oncology.
Wnt Ligands
Wnt1: Often overexpressed in breast cancer and some types of leukemia.
Wnt Receptors
Frizzled (Fzd) Receptors: Different Fzd receptors (e.g., Fzd1, Fzd2, Fzd7) have been implicated in various cancers:
Fzd1: Overexpressed in colorectal cancer.
Fzd2: Associated with breast cancer and prostate cancer.
Fzd7: Linked to gastric cancer and glioblastoma.
Scientific Papers found: Click to Expand⟱
6040- CGA,    Protective effect of chlorogenic acid on cognitive impairment in rats with early Alzheimer's disease via Wnt signaling pathway
- in-vivo, AD, NA
*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↓,

3205- EGCG,    The Role of Epigallocatechin-3-Gallate in Autophagy and Endoplasmic Reticulum Stress (ERS)-Induced Apoptosis of Human Diseas
- Review, Var, NA - Review, AD, NA
Beclin-1↑, EGCG not only regulates autophagy via increasing Beclin-1 expression and reactive oxygen species generation,
ROS↑,
Apoptosis↑, Apoptosis is a common cell function in biology and is induced by endoplasmic reticulum stress (ERS)
ER Stress↑,
*Inflam↓, EGCG has health benefits including anti-tumor [15], anti-inflammatory [16], anti-diabetes [17], anti-myocardial infarction [18], anti-cardiac hypertrophy [19], anti-atherosclerosis [20], and antioxidant
*cardioP↑,
*antiOx↑,
*LDL↓, These effects are mainly related to (LDL) cholesterol inhibition, NF-κB inhibition, MPO activity inhibition, decreased levels of glucose and glycated hemoglobin in plasma, decreased inflammatory markers, and reduced ROS generation
*NF-kB↓,
*MPO↓,
*glucose↓,
*ROS↓,
ATG5↑, EGCG induced autophagy by enhancing Beclin-1, ATG5, and LC3B and promoted mitochondrial depolarization in breast cancer cells.
LC3B↑,
MMP↑,
lactateProd↓, 20 mg kg−1 EGCG significantly decreased glucose, lactic acid, and vascular endothelial growth factor (VEGF) levels
VEGF↓,
Zeb1↑, (20 uM) inhibited the proliferation through activating autophagy via upregulating ZEB1, WNT11, IGF1R, FAS, BAK, and BAD genes and inhibiting TP53, MYC, and CASP8 genes in SSC-4 human oral squamous cells [
Wnt↑,
IGF-1R↑,
Fas↑,
Bak↑,
BAD↑,
TP53↓,
Myc↓,
Casp8↓,
LC3II↑, increasing the LC3-II expression levels and induced apoptosis via inducing ROS in mesothelioma cell lines,
NOTCH3↓, but also could reduce partially Notch3/DLL3 to reduce drug-resistance and the stemness of tumor cells
eff↑, In combination therapies, low-intensity pulsed electric field (PEF) can improve EGCG to affect tumor cells; ultrasound (US) with tumor cells is the application of physical stimulation in cancer therapy.
p‑Akt↓, 20 μM EGCG increased intracellular ROS levels and LC3-II, and inhibited p-Akt in PANC-1 cells
PARP↑, 100 μM EGCG increased LC3-II, activated caspase-3 and PARP, and reduced p-Akt in HepG2
*Cyt‑c↓, EGCG protected neuronal cells against human viruses by inhibiting cytochrome c and Bax translocations, and reducing autophagy with increased LC3-II expression and decreased p62 expression
*BAX↓,
*memory↑, EGCG restored autophagy in the mTOR/p70S6K pathway to weaken memory and learning disorders induced by CUMS
*neuroP↑, Finally, EGCG increased the neurological scores through inhibiting cell death
*Ca+2?, EGCG treatment, [Ca2+]m and [Ca2+]i expressions were reduced and oxyhemoglobin-induced mitochondrial dysfunction lessened.
GRP78/BiP↑, MMe cells with EGCG treatment improved GRP78 expression in the endoplasmic reticulum, and induced EDEM, CHOP, XBP1, and ATF4 expressions, and increased the activity of caspase-3 and caspase-8.
CHOP↑, GRP78 accumulation converted UPR of MMe cells into pro-apoptotic ERS
ATF4↑,
Casp3↑,
Casp8↑,
UPR↑,

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
*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, 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

218- MFrot,  MF,    Extremely low frequency magnetic fields inhibit adipogenesis of human mesenchymal stem cells
- in-vitro, Nor, NA
*PPARγ↓, PPARg2
*p‑JNK↑, p-JNK
*Wnt↑,
*ALP∅, ELF-MF had no effects on the expression of ALP, COL1a1, Runx2, and OCN
*COL1∅,
*RUNX2∅,
*OCN∅,
*FABP4↓, ELF-MF exposure for 15 days resulted in a decrease in PPARg2 and FABP4
*p‑JNK↑, p-JNK was increased after ELF-MF exposure
*Diff↓, adipogenic differentiation of MSCs could be inhibited by ELF-MF of 7.5 Hz, 0.4 T, suggesting the inhibitory effect of ELF-MF on obesity may be attributed to the inhibition of differentiation of MSCs into adipocytes.


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,  

Core Metabolism/Glycolysis ⓘ

lactateProd↓, 1,  

Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 2,   BAD↑, 1,   Bak↑, 1,   Casp3↑, 1,   Casp8↓, 1,   Casp8↑, 1,   Fas↑, 1,   MAPK↑, 1,   Myc↓, 1,   Necroptosis↑, 1,   p38↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3B↑, 1,   LC3II↑, 1,  

DNA Damage & Repair ⓘ

PARP↑, 1,   TP53↓, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   IGF-1R↑, 1,   NOTCH3↓, 1,   Wnt↑, 1,  

Migration ⓘ

Ca+2↑, 2,   TumCP↓, 1,   Zeb1↑, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

ATF4↑, 1,   NO↑, 1,   VEGF↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 1,   eff↑, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

Myc↓, 1,   TP53↓, 1,  
Total Targets: 42

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   MPO↓, 1,   NRF2↑, 1,   ROS↓, 2,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,  

Core Metabolism/Glycolysis ⓘ

FABP4↓, 1,   glucose↓, 1,   LDL↓, 1,   PPARγ↓, 1,  

Cell Death ⓘ

BAX↓, 1,   Cyt‑c↓, 1,   p‑JNK↑, 2,  

Kinase & Signal Transduction ⓘ

OCN∅, 1,  

Proliferation, Differentiation & Cell State ⓘ

Diff↓, 1,   Diff↑, 1,   GSK‐3β↓, 1,   RUNX2∅, 1,   Wnt↑, 4,  

Migration ⓘ

Ca+2?, 1,   Ca+2↑, 2,   COL1∅, 1,   FAK↑, 1,   β-catenin/ZEB1↑, 3,  

Angiogenesis & Vasculature ⓘ

angioG↑, 1,   VEGF↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Synaptic & Neurotransmission ⓘ

tau↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   eff↝, 1,  

Clinical Biomarkers ⓘ

ALP∅, 1,   BMD↑, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 1,   memory↑, 2,   neuroP↑, 2,  
Total Targets: 37

Scientific Paper Hit Count for: Wnt, Wingless-related integration site
3 Magnetic Fields
1 Chlorogenic acid
1 EGCG (Epigallocatechin Gallate)
1 Magnetic Field Rotating
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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