Treg lymp Cancer Research Results

Treg lymp, Treg lymphocytes: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Regulatory T cells (Tregs) are a subset of T lymphocytes that play a crucial role in maintaining immune tolerance and preventing autoimmune diseases. They are characterized by the expression of specific markers, such as CD4, CD25, and the transcription factor FoxP3.
Tregs are often found in high numbers within the tumor microenvironment. Their presence can suppress anti-tumor immune responses, allowing cancer cells to evade immune detection and destruction. By inhibiting the activity of effector T cells and other immune components, Tregs can promote tumor growth and metastasis.
Scientific Papers found: Click to Expand⟱
560- ART/DHA,    Dihydroartemisinin shift the immune response towards Th1, inhibit the tumor growth in vitro and in vivo
- in-vivo, NA, NA
IL4↓,
CD4+↓,
CD25+↓,
FoxP3+↓, Foxp3+
Treg lymp↓,

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↓,

1863- dietFMD,  Chemo,    Effect of fasting on cancer: A narrative review of scientific evidence
- Review, Var, NA
eff↑, recommend combining prolonged periodic fasting with a standard conventional therapeutic approach to promote cancer‐free survival, treatment efficacy, and reduce side effects in cancer patients.
ChemoSideEff↓, lowered levels of IGF1 and insulin have the potential to protect healthy cells from side effects
ChemoSen↑,
Insulin↓, causes insulin levels to drop and glucagon levels to rise
HDAC↓, Histone deacetylases are inhibited by ketone bodies, which may slow tumor development.
IGF-1↓, FGF21 rises during intermittent fasting, and it plays a vital role in lowering IGF1 levels by inhibiting phosphorylated STAT5 in the liver
STAT5↓,
BG↓, Fasting suppresses glucose, IGF1, insulin, the MAPK pathway, and heme oxygenase 1
MAPK↓,
HO-1↓,
ATG3↑, while increasing many autophagy‐regulating components (Atgs, LC3, Beclin1, p62, Sirt1, and LAMP2).
Beclin-1↑,
p62↑,
SIRT1↑,
LAMP2↑,
OXPHOS↑, Fasting causes cancer cells to release oxidative phosphorylation (OXPHOS) through aerobic glycolysis
ROS↑, which leads to an increase in reactive oxygen species (ROS), p53 activation, DNA damage, and cell death in response to chemotherapy.
P53↑,
DNAdam↑,
TumCD↑,
ATP↑, and causes extracellular ATP accumulation, which inhibits Treg cells and the M2 phenotype while activating CD8+ cytotoxic T cells.
Treg lymp↓,
M2 MC↓,
CD8+↑,
Glycolysis↓, By lowering glucose intake and boosting fatty acid oxidation, fasting can induce a transition from aerobic glycolysis to mitochondrial oxidative phosphorylation in cancerous cells, resulting in increased ROS
GutMicro↑, Fasting has been shown to have a direct impact on the gut microbial community's constitution, function, and interaction with the host, which is the complex and diverse microbial population that lives in the intestine
GutMicro↑, Fasting also reduces the number of potentially harmful Proteobacteria while boosting the levels of Akkermansia muciniphila.
Warburg↓, Fasting generates an anti‐Warburg effect in colon cancer models, which increases oxygen demand but decreases ATP production, indicating an increase in mitochondrial uncoupling.
Dose↝, Those patients fasted for 36 h before treatment and 24 h thereafter, having a total of 350 calories per day. Within 8 days of chemotherapy, no substantial weight loss was recorded, although there was an improvement in quality of life and weariness.

1038- F,  immuno,    Fucoidan enhances the anti-tumor effect of anti-PD-1 immunotherapy by regulating gut microbiota.
- in-vivo, BC, NA
GutMicro↑, ucoidan significantly improved the composition of the gut microbiota by increasing the number of potentially beneficial bacteria, such as Bifidobacterium, Faecalibaculum and Lactobacillus.
T-Cell↑, improved the function of effector T cells
Treg lymp↓,

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↑,

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

228- MFrot,  MF,    Rotating magnetic field ameliorates experimental autoimmune encephalomyelitis by promoting T cell peripheral accumulation and regulating the balance of Treg and Th1/Th17
- NA, MS, NA
*CD4+↑, RMF (0.2 T, 4 Hz) treatment increases the accumulation of CD4+ cells in the spleen and lymph nodes
*MCP1↓, by downregulating the expression of CCL-2, CCL-3 and CCL-5
RANTES↓,
*MIP‑1α↓,
*Treg lymp↓, increasing the proportion of Treg cells
*IFN-γ↓, However, on day 20 after immunization, IFN-γ and IL-17A levels in the serum of EAE mice were significantly reduced by the exposure of RMF
*IL17↓,
*CXCc↓, mRNA expression of IFN chemokines (CXCL-1 and CXCL-2), and IL-17 chemokines (CXCL-9 and CXCL-10) had also significantly reduced in EAE mice after RMF exposure.

1798- NarG,    Naringenin: A potential flavonoid phytochemical for cancer therapy
- Review, NA, NA
*Inflam↓, including anti-inflammatory, antioxidant, neuroprotective, hepatoprotective, and anti-cancer activities
*antiOx↓,
neuroP↑, neuroprotective
hepatoP↑, hepatoprotective
AntiCan↑,
Apoptosis↑, apoptosis induction, cell cycle arrest, angiogenesis hindrance
TumCCA↑,
angioG↓,
ROS↝, antioxidant effects, by modulating reactive oxygen species (ROS) levels and increasing superoxide dismutase (SOD
SOD↑,
TGF-β↓, inhibition of transforming growth factor-β (TGF-β), suppression of regulatory T-cells (Tregs), and down-regulation of interleukin-1β (IL-1β)
Treg lymp↓,
IL1β↓,
*BioAv↝, naringenin is mainly responsible for its low aqueous solubility, low oral bioavailability, and instability which are challenges to its efficient medical application. To overcome these physicochemical issues, nano-drug delivery systems have been used
ChemoSen↑, ombinational therapy consisting of naringenin and standard anti-cancer agents is arising, as a new treatment strategy and was proven to show synergistic effects
cardioP↑, cardioprotective

4853- Uro,    Urolithin A, a novel natural compound to target PI3K/AKT/mTOR pathway in pancreatic cancer
- vitro+vivo, PC, MIA PaCa-2 - in-vitro, NA, PANC1
p‑Akt↓, treatment of PDAC cells with Uro A blocked the phosphorylation of AKT and p70S6K in vitro, successfully inhibited the growth of tumor xenografts, and increased overall survival (OS)
p‑p70S6↓,
TumCG↓,
OS↑,
PI3K↓, Uro A as a therapeutic agent in PDAC through suppression of the PI3K/AKT/mTOR pathway.
mTOR↓,
TumCP↓, Uro A treatment inhibits PDAC cell proliferation, migration, and enhances apoptosis
TumCMig↓,
Apoptosis↑,
TAMS↓, Improved therapeutic response to Uro A treatment is associated with a reduction in immunosuppressive tumor- associated macrophages (TAMs) and regulatory T cells (Tregs) in PKT mice
Treg lymp↓,
Wnt↓, Uro A is known to mediate its anti-tumor activities through downregulation of Wnt and IGF-1 signaling in colon and prostate cancer cells
IGF-1↓,
*toxicity↓, A Phase I clinical trial of Uro A demonstrated that it is well-tolerated with good bioavailability
*BioAv↑,
Half-Life↝, Uro A is rapidly absorbed and reaches peak plasma concentration two hours after ingestion


Showing Research Papers: 1 to 9 of 9

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 9

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↓, 1,   OXPHOS↑, 1,   ROS↑, 1,   ROS↝, 1,   SOD↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   Insulin↓, 1,  

Core Metabolism/Glycolysis ⓘ

CAIX↑, 1,   Glycolysis↓, 1,   SIRT1↑, 1,   Warburg↓, 2,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   p27↑, 1,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

p‑p70S6↓, 1,  

Autophagy & Lysosomes ⓘ

ATG3↑, 1,   Beclin-1↑, 1,   LAMP2↑, 1,   p62↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNArepair↑, 1,   P53↑, 2,  

Cell Cycle & Senescence ⓘ

CDK4↓, 2,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   IGF-1↓, 2,   IGF-1R↓, 1,   mTOR↓, 1,   PI3K↓, 2,   PTEN↑, 1,   STAT3↓, 1,   p‑STAT3↓, 1,   STAT5↓, 1,   TumCG↓, 1,   TumCG↑, 1,   Wnt↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   MMP13↓, 1,   MMP2↓, 1,   MMP9↓, 1,   TGF-β↓, 1,   Treg lymp↓, 8,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↑, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,   NO↓, 1,   TAMS↓, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

GLUT1↑, 1,   GLUT3↑, 1,  

Immune & Inflammatory Signaling ⓘ

CD25+↓, 2,   CD4+↓, 2,   CD4+↑, 1,   COX2↓, 2,   FOXP3↓, 3,   FoxP3+↓, 2,   IFN-γ↑, 1,   IL1β↓, 1,   IL4↓, 1,   IL6↓, 1,   IL8↓, 1,   M2 MC↓, 1,   NF-kB↓, 1,   NK cell↑, 1,   PGE2↓, 1,   RANTES↓, 1,   T-Cell↑, 2,   Th1 response↑, 1,   TNF-α↑, 1,  

Hormonal & Nuclear Receptors ⓘ

RANKL↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,   ChemoSen↑, 3,   Dose↝, 1,   Dose∅, 1,   eff↑, 2,   Half-Life↝, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,   GutMicro↑, 3,   IL6↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   cardioP↑, 1,   ChemoSideEff↓, 2,   hepatoP↑, 1,   neuroP↑, 1,   OS↑, 2,   radioP↑, 1,  

Infection & Microbiome ⓘ

CD8+↑, 2,  
Total Targets: 103

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

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

Migration ⓘ

Treg lymp↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   CXCc↓, 1,   IFN-γ↓, 1,   IL17↓, 1,   Inflam↓, 1,   MCP1↓, 1,   MIP‑1α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 17

Scientific Paper Hit Count for: Treg lymp, Treg lymphocytes
2 Artemisinin
2 immunotherapy
1 diet FMD Fasting Mimicking Diet
1 Chemotherapy
1 Fucoidan
1 Gallic acid
1 Melatonin
1 Magnetic Field Rotating
1 Magnetic Fields
1 Naringin
1 Urolithin
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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