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⟱
7489- H2,    Molecular Hydrogen in the Treatment of Respiratory Diseases
- Review, Asthma, NA
*antiOx↑, Molecular hydrogen is gaining increasing attention as an antioxidant, anti-inflammatory, and antiapoptotic agent.
*Inflam↓,
*Apoptosis↓,
*Dose↓, It reaches a maximum level of about 0.78 mM (≈1.6 mg/L) at room temperature with a loss of about 2–5% per 3 min
*Dose↝, It is produced (and consumed) by bacteria of the gut microbiota .The most prominent bacterial phyla involved in this process are the Firmicutes and Bacteroidetes phyla, which include the anaerobic Clostridium species
*eff↑, hydrogen mixed with oxygen at a ratio of 96%-to-4%, known as the Hydrox gas mixture, was used by deep-sea divers to prevent decompression sickness and allow diving to depths of up to 500 m
*ROS↓, The antioxidant activity of H2 is based on two processes: a direct scavenging of the most toxic reactive oxygen and nitrogen species (ROS/RNS),
*RNS↓,
*NRF2↑, H2 activates the Nrf2 (nuclear factor erythroid 2-related factor 2) pathway, a key transcription factor involved in oxidative stress-related responses, including cytoprotective, antioxidant, and detoxifying enzymes such as HO-1
*HO-1↑,
*Fenton↓, removal of free heme and inhibition of the Fenton reaction
*NLRP3↓, the activation of the Nrf2 pathway has been shown to inhibit the NLRP3 (NLR family pyrin domain containing 3) inflammasome,
*NADPH↓, H2 suppresses the activation of the NADPH oxidase pathway and downregulates the expression of NOX2 and NOX4
*NOX4↓,
*NOX↓,
*MPO↓, H2 has been shown to reduce the overactivation of myeloperoxidase (MPO)
*NF-kB↓, would further suppress the NFκB
*TNF-α↓, figure 3
*IL6↓,
*IL1β↓,
*HMGB1↓,
*IL4↑,
*IL10↑,
*M2 MC↑, Additionally, H2 promotes the polarization of macrophages from the proinflammatory M1 type to the anti-inflammatory M2 type
*Treg lymp↝, It also inhibits Th2 responses, restores regulatory T cells (Treg), and, thus, normalizes an overactivated immune system
*Bcl-2↑, upregulate the antiapoptotic factors, including Bcl-2 and Bcl-xl.
*Bcl-xL↑,
*PI3K↑, phenomenon is likely facilitated by the activation of the PI3K/Akt and JAK2/STAT3 signaling pathways
*Akt↑,
*JAK2↑,
*STAT3↑,
*Dose↑, The consumption of certain prebiotics, especially those rich in dietary fiber, indigestible starches, and sugars (lactulose), has been demonstrated to enhance intestinal H2 production through the activity of intestinal flora
*CD4+↑, H2 increased the population of CD4+CD25+Foxp3+ Treg cells, which are often decreased in allergic rhinitis (AR)
*CD25+↑,
*FOXP3↑,
*MDA↓, H2 administration attenuated oxidative stress expressed as lower MDA and other lipid peroxidation markers along with an enhancement in the expression and activity of endogenous antioxidant enzymes such as SOD or CAT
*SOD↑,
*Catalase↑,
*Casp3↓, inhibition of proapoptotic processes like the caspase 3 and 9 pathways
*Casp9↓,
*TBARS↓, drinking of HRW by patients with asthma and COPD leads to an increase in blood oxygen saturation, vitamin E levels, along with lower oxidative stress markers such as thiobarbituric acid reactive substances (TBARS), MDA,
*SpO2↑,
*VitE↓,
*OS↑, COPD:In general, H2 administration has been found to lead to enhanced survival and reduced weight loss [110], improved lung function and static lung compliance, and decreased arterial blood pressure
*Weight↑,
*DNAdam↓, reduction in levels of oxidative DNA damage markers
*PGE2↓, H2 reduced elevated inflammatory markers, including IL-1β, IL-6, TNF-α, prostaglandin E2 (PGE2) [29,65,71,128,130], macrophage protein 1α 2 (MP1α), and monocyte chemoattractant protein-1 (MCP-1)
*MCP1/CCL2↓,
*lipid-P↓, Further, a reduction in oxidative stress markers such as lipid peroxidation and proapoptotic markers, including Bax and caspase-3, was observed.
*TumCP↓, H2-rich medium reduced the colony size and formation of tongue cancer cells and decreased proliferation in human fibrosarcoma and esophageal cancer cells, as well as A549 cells
*tumCV↓, decrease in cell viability, migration, and invasion
*TumCMig↓,
*TumCI↓,
TumW↓, A reduction in tumor weight and size, as well as a lower number of cells of squamous cell carcinoma, was revealed by animal studies.
TumVol↓,
selectivity↑, Notably, as previously reported, H2 administration exhibited no effect on healthy animals or non-cancerous cell lines
QoL↑, Patients reported improved quality of life with better physical status and fewer pulmonary symptoms
ChemoSen↑, In combination with conventional (such as cis-platin) and modern (including antibodies like nivolumab) therapeutics, H2 enhanced drug activity, resulting in enhanced outcomes and improved disease control
chemoP↑, and reduced side effects of the treatment, such as nephrotoxicity, weight loss, insomnia, pain, or hearing loss in the case of radiotherapy
radioP↑, radioprotective effects of H2 are primarily attributed to its hydroxyl radical scavenging activity
ROS↑, As indicated by Yang et al., the latter include the activation of the ROS/NLRP3/caspase-3/gasdermin D-mediated pyroptotic pathways
NLRP3↑,
Casp3↑,
VEGF↓, suppression of vascular endothelial growth factor (VEGF) expression
Wnt↓, H2 result in the suppression of the overactivated Wnt/beta-catenin signaling pathways, which further leads to suppression of tumor progression
β-catenin/ZEB1↓,

4220- PI,    Piperine ameliorated memory impairment and myelin damage in lysolecethin induced hippocampal demyelination
- in-vivo, AD, NA - in-vivo, MS, NA
*memory↑, piperine improved the memory performance and myelin repair in the hippocampal demyelination model
*iNOS↓, Piperine inhibited iNOS expression concomitant with enhanced expression levels of Nrf2, HO1 and the total antioxidant capacity in the hippocampal tissue.
*NRF2↑,
*HO-1↑,
*TAC↑,
*TNF-α↓, Piperine treatment significantly reduced the gene expression level of TNF-α, IL1-β, NF-κB, and glial activation in the injured area;
*IL1β↓,
*NF-kB↓,
*IL10↑, however, the mRNA level of IL-10, Foxp3, BDNF and MBP were significantly increased
*FOXP3↑,
*BDNF↑,
other↑, piperine as a promising therapeutic target in MS patients


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

ROS↑, 1,  

Cell Death(tgid=5) ⓘ

Casp3↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,  

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

Wnt↓, 1,  

Migration(tgid=13) ⓘ

β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGF↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↑, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   selectivity↑, 1,  

Functional Outcomes(tgid=23) ⓘ

chemoP↑, 1,   QoL↑, 1,   radioP↑, 1,   TumVol↓, 1,   TumW↓, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

SpO2↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   Fenton↓, 1,   HO-1↑, 2,   lipid-P↓, 1,   MDA↓, 1,   MPO↓, 1,   NOX4↓, 1,   NRF2↑, 2,   RNS↓, 1,   ROS↓, 1,   SOD↑, 1,   TAC↑, 1,   TBARS↓, 1,   VitE↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

NADPH↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 1,   Apoptosis↓, 1,   Bcl-2↑, 1,   Bcl-xL↑, 1,   Casp3↓, 1,   Casp9↓, 1,   iNOS↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

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

PI3K↑, 1,   STAT3↑, 1,  

Migration(tgid=13) ⓘ

Treg lymp↝, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD25+↑, 1,   CD4+↑, 1,   FOXP3↑, 2,   HMGB1↓, 1,   IL10↑, 2,   IL1β↓, 2,   IL4↑, 1,   IL6↓, 1,   Inflam↓, 1,   JAK2↑, 1,   M2 MC↑, 1,   MCP1/CCL2↓, 1,   NF-kB↓, 2,   PGE2↓, 1,   TNF-α↓, 2,  

Cellular Microenvironment(tgid=17) ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

BDNF↑, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

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

Clinical Biomarkers(tgid=22) ⓘ

IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

memory↑, 1,   OS↑, 1,   Weight↑, 1,  
Total Targets: 58

Scientific Paper Hit Count for: FOXP3, forkhead box P3
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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