FOXP3 Cancer Research Results

FOXP3, forkhead box P3: Click to Expand ⟱
Source:
Type: TSG (not)
Also known as scurfin
FOXP3 (Forkhead box P3) is a transcription factor that serves as the master regulator of regulatory T cells (Tregs)
Immune Suppression, Tregs, and Context-Dependent Tumor Biology
Forkhead box P3 (FOXP3), an X-linked tumor suppressor gene.
appears to function as a master regulator of the regulatory pathway in the development and function of regulatory T cells.
FOXP3 can promote the apoptosis of breast cancer cells by upregulating the expression of PDCD4, thus exerting a tumor suppressive function.
Increasing evidence has shown that FOXP3 is also expressed in tumor cells. However, the results of tumor FOXP3 is inconsistent and even the opposite. In some types of human cancers, the expression of FOXP3 is upregulated, and it can promote the development of cancers, leading to a poor prognosis. While in some other types of cancers, it is a different story. The reason for the contradictory data is unknown.

Expression: FOXP3 is expressed in Tregs within the tumor microenvironment.
Prognosis: High FOXP3 expression can correlate with poor prognosis, as it may indicate immune evasion by the tumor.(but not always)
Scientific Papers found: Click to Expand⟱
562- ART/DHA,    Artesunate exerts an anti-immunosuppressive effect on cervical cancer by inhibiting PGE2 production and Foxp3 expression
- in-vivo, NA, HeLa
CD4+↓,
CD25+↓,
FoxP3+↓,
Treg lymp↓,
PGE2↓,
FOXP3↓,
COX2↓,

1283- GA,  immuno,    Gallic acid induces T-helper-1-like Treg cells and strengthens immune checkpoint blockade efficacy
- vitro+vivo, CRC, NA
p‑STAT3↓,
Treg lymp↓,
FOXP3↓,
CD8+↑,
IFN-γ↑,

4516- MAG,    Magnolol Induces Apoptosis and Suppresses Immune Evasion in Non-small Cell Lung Cancer Xenograft Models
- in-vivo, NSCLC, NA
selectivity↑, suppressed NSCLC progression, with no pathology alterations observed in normal organs
Apoptosis↑, Magnolol-induced apoptosis and cell cycle arrest, evidenced by increased cleaved caspase-3 and decreased cyclin D1/CDK4 levels.
TumCCA↑,
Casp3↑,
cycD1/CCND1↓,
CDK4↓,
VEGF↓, down-regulated VEGF, FOXP3, and IDO-1 in tumors, implicating tumor microenvironment modulation.
FOXP3↓,
IDO1↓,

1782- MEL,    Melatonin in Cancer Treatment: Current Knowledge and Future Opportunities
- Review, Var, NA
AntiCan↑, involvement of melatonin in different anticancer mechanisms
Apoptosis↑, apoptosis induction, cell proliferation inhibition, reduction in tumor growth and metastases
TumCP↓,
TumCG↑,
TumMeta↑,
ChemoSideEff↓, reduction in the side effects associated with chemotherapy and radiotherapy, decreasing drug resistance in cancer therapy,
radioP↑,
ChemoSen↑, augmentation of the therapeutic effects of conventional anticancer therapies
*ROS↓, directly scavenge ROS and reactive nitrogen species (RNS)
*SOD↑, melatonin can regulate the activities of several antioxidant enzymes like superoxide dismutase, glutathione reductase, glutathione peroxidase, and catalase
*GSH↑,
*GPx↑,
*Catalase↑,
Dose∅, demonstrated that 1 mM melatonin concentration is the pharmacological concentration that is able to produce anticancer effects
VEGF↓, downregulatory action on VEGF expression in human breast cancer cells
eff↑, tumor-bearing mice were treated with (10 mg/kg) of melatonin and (5 mg/kg) of cisplatin. The results have shown that melatonin was able to reduce DNA damage
Hif1a↓, MDA-MB-231-downregulation of the HIF-1α gene and protein expression coupled with the production of GLUT1, GLUT3, CA-IX, and CA-XII
GLUT1↑,
GLUT3↑,
CAIX↑,
P21↑, upregulation of p21, p27, and PTEN protein is another way of melatonin to promote cell programmed death in uterine leiomyoma
p27↑,
PTEN↑,
Warburg↓, FIGURE 3
PI3K↓, in colon cancer cells by downregulation of PI3K/AKT and NF-κB/iNOS
Akt↓,
NF-kB↓,
cycD1/CCND1↓,
CDK4↓,
CycB/CCNB1↓,
CDK4↓,
MAPK↑,
IGF-1R↓,
STAT3↓,
MMP9↓,
MMP2↓,
MMP13↓,
E-cadherin↑,
Vim↓,
RANKL↓,
JNK↑,
Bcl-2↓,
P53↑,
Casp3↑,
Casp9↑,
BAX↑,
DNArepair↑,
COX2↓,
IL6↓,
IL8↓,
NO↓,
T-Cell↑,
NK cell↑,
Treg lymp↓,
FOXP3↓,
CD4+↑,
TNF-α↑,
Th1 response↑, FIGURE 3
BioAv↝, varies 1% to 50%?
RadioS↑, melatonin’s radio-sensitizing properties
OS↑, In those individuals taking melatonin, the overall tumor regression rate and the 5-year survival were elevated

225- MFrot,  MF,    Extremely low frequency magnetic fields regulate differentiation of regulatory T cells: Potential role for ROS-mediated inhibition on AKT
- vitro+vivo, Lung, NA
MMP2↓,
MMP9↓,
FOXP3↓,
ROS↑,
p‑Akt↓,

1489- RES,    Molecular mechanisms of resveratrol as chemo and radiosensitizer in cancer
- Review, Var, NA
RadioS↑,
ChemoSen↑,
*BioAv↓, However, in vivo experimental models have demonstrated that RSV is rapidly metabolized and eliminated, which leads to low bioavailability of the compound. 75% of RSV has been shown to be absorbed orally, only 1% is detected in the blood plasma
*BioAv↑, nanocarrier of RSV-loaded poly (ε-caprolactone)-poly (ethylene glycol) nanoparticles with an erythrocyte membrane. This system improved RSV’s poor water solubility
Ferroptosis↑, SV could induce ferroptotic cell death in colorectal cancer by initiating lipid peroxidation and suppressing the expression of SLC7A11 and GPX4
lipid-P↑,
xCT↓,
GPx4↓,
*BioAv↑, Bioactive or bioenhancer compounds have also been used (piperine, quercetin, biflavone ginkgetin) that, in combination with RSV, improve bioavailability, solubility, absorption, and cellular permeability
COX2↓, inhibiting Cyclooxygenase-COX
cycD1/CCND1↓,
FasL↓,
FOXP3↓,
HLA↑,
p‑NF-kB↓, decrease NF-ĸB phosphorylation
BAX↑,
Bcl-2↓,
MALAT1↓, decrease the expression of the lncRNA MALAT1 in colorectal and gastric cancer cells through the Wnt/β-catenin signaling pathway


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   lipid-P↑, 1,   ROS↑, 1,   xCT↓, 1,  

Core Metabolism/Glycolysis ⓘ

CAIX↑, 1,   IDO1↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 2,   Bcl-2↓, 2,   Casp3↑, 2,   Casp9↑, 1,   FasL↓, 1,   Ferroptosis↑, 1,   JNK↑, 1,   MAPK↑, 1,   p27↑, 1,  

DNA Damage & Repair ⓘ

DNArepair↑, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 3,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,   PI3K↓, 1,   PTEN↑, 1,   STAT3↓, 1,   p‑STAT3↓, 1,   TumCG↑, 1,  

Migration ⓘ

E-cadherin↑, 1,   HLA↑, 1,   MALAT1↓, 1,   MMP13↓, 1,   MMP2↓, 2,   MMP9↓, 2,   Treg lymp↓, 3,   TumCP↓, 1,   TumMeta↑, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 1,   NO↓, 1,   VEGF↓, 2,  

Barriers & Transport ⓘ

GLUT1↑, 1,   GLUT3↑, 1,  

Immune & Inflammatory Signaling ⓘ

CD25+↓, 1,   CD4+↓, 1,   CD4+↑, 1,   COX2↓, 3,   FOXP3↓, 6,   FoxP3+↓, 1,   IFN-γ↑, 1,   IL6↓, 1,   IL8↓, 1,   NF-kB↓, 1,   p‑NF-kB↓, 1,   NK cell↑, 1,   PGE2↓, 1,   T-Cell↑, 1,   Th1 response↑, 1,   TNF-α↑, 1,  

Hormonal & Nuclear Receptors ⓘ

RANKL↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   ChemoSen↑, 2,   Dose∅, 1,   eff↑, 1,   RadioS↑, 2,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   ChemoSideEff↓, 1,   OS↑, 1,   radioP↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 1,  
Total Targets: 77

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

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

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 2,  
Total Targets: 7

Scientific Paper Hit Count for: FOXP3, forkhead box P3
1 Artemisinin
1 Gallic acid
1 immunotherapy
1 Magnolol
1 Melatonin
1 Magnetic Field Rotating
1 Magnetic Fields
1 Resveratrol
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#:581  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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