FOXO1 Cancer Research Results

FOXO1, Forkhead box O1: Click to Expand ⟱
Source:
Type:
FOXO-1 contributes to cellular homeostasis by regulating genes involved in apoptosis, cell cycle arrest, and metabolism.

– In many cancers, FOXO-1 activity can be reduced via genetic or epigenetic mechanisms, altered subcellular localization (e.g., cytoplasmic sequestration following phosphorylation by Akt), or protein degradation.
– This loss of nuclear FOXO-1 activity is often associated with diminished tumor suppressor functions.
– Decreased nuclear FOXO-1 expression or activity correlates with higher tumor grade and poorer prognosis.

– FOXO-1 is a key downstream target of the PI3K/Akt pathway. Hyperactivation of Akt, common in many cancers, leads to FOXO-1 inactivation.
Scientific Papers found: Click to Expand⟱
3433- ALA,    Alpha lipoic acid promotes development of hematopoietic progenitors derived from human embryonic stem cells by antagonizing ROS signals
*ROS↓, However, in more mature hPSC‐derived hematopoietic stem/progenitor cells, ALA reduced ROS levels and inhibited apoptosis.
*Apoptosis↓,
*Hif1a↑, up‐regulating HIF1A in response to a hypoxic environment.
*FOXO1↑, ALA also up‐regulated sensor genes of ROS signals, including HIF1A, FOXO1, FOXO3, ATM, PETEN, SIRT1, and SIRT3, during the process of hPSCs derived hemogenic endothelial cells generation
*FOXO3↑,
*ATM↑,
*SIRT1↑,
*SIRT3↑,
*CD34↑, Flow cytometry analysis indicated that ALA improved the production of CD34+ CD43+ CD45+ hematopoietic stem/progenitor cells significantly

5692- BJ,    Seed oil of Brucea javanica induces apoptosis through the PI3K/Akt signaling pathway in acute lymphocytic leukemia Jurkat cells
- vitro+vivo, AML, NA
Apoptosis↑, BJOE induced apoptosis in Jurkat cells and were suggestive of intrinsic apoptotic induction
Akt↓, BJOE inhibited Akt (protein kinase B) activation and upregulated its downstream targets p53 and FoxO1 (forkhead box gene, group O-1) to initiate apoptosis
P53↑,
FOXO1↑,
GSK‐3β↑, The activation of GSK3β was also involved.
TumVol↓, In a 96-case clinical trial, BJOE treatment reduced tumor size and improved the quality of life for patients with gastrointestinal cancer and cervical cancer [18].
QoL↑,
BBB↑, As shown in pharmacokinetic studies, BJOE crossed the blood-brain barrier
OS↑, In another 100-case clinical trial, BJOE prolonged the survival of patients with brain meta- stases from lung cancer [24].
Dose↝, Currently, BJOE is intravenously administered for the clinical treatment of lung cancer [25-28] and gastric cancer [29-31]
MMP↓, MMP collapse and ROS production in Jurkat cells were also observed following BJOE treatment.
ROS↑,
XIAP↑, we found that BJOE targeted Akt to stimulate FoxO1 and XIAP to induce apoptosis.
Casp9↑, BJOE promoted the activation of caspase- 9, caspase-8 and caspase-3.
Casp8↑,
Casp3↑,
cl‑PARP↑, The cleavage of PARP proteins was also observed.
TumCCA↑, the sub-G1 phase cell percentages increased in all five samples in a BJOE concentration-dependent manner.

3246- EGCG,    Epigallocatechin gallate suppresses hepatic cholesterol synthesis by targeting SREBP-2 through SIRT1/FOXO1 signaling pathway
- in-vitro, Nor, NA
*MDA↓, EGCG remarkably diminished MDA content in the liver with hypercholesterolemia and increased T-AOC and SOD activity.
*SOD↑,
*SIRT1↑, EGCG activated SIRT1 and increased FOXO1 expression
*FOXO1↑,
*SREBP2↓, EGCG increased FOXO1 expression, and decrease SREBP-2 expression

1678- PBG,  5-FU,  sericin,    In vitro and in vivo anti-colorectal cancer effect of the newly synthesized sericin/propolis/fluorouracil nanoplatform through modulation of PI3K/AKT/mTOR pathway
- in-vitro, CRC, Caco-2 - in-vivo, NA, NA
PI3K↓, mechanism of action of the prepared nanoformula revealed that it acts through the inhibition of the PI3K/AKT/mTOR signaling pathway and consequently inhibiting cancerous cells proliferation.
Akt↓,
mTOR↓,
TumCP↓,
Bcl-2↓, downregulated BCL2 (B-cell lymphoma 2) and activated BAX, Caspase 9 and Caspase 3 expression
BAX↑,
Casp3↑,
Casp9↑,
ROS↓, prepared nanoformula decreased the ROS (Reactive Oxygen Species) production in vivo owing to PI3K/AKT/mTOR pathway inhibition and FOXO-1 (Forkhead Box O1) activation
FOXO1↑,
*toxicity∅, LD50 of the prepared nanoformula reached 1 mg/Kg upon oral administration.
eff↑, It is well known that propolis and sericin inhibit PI3K/AKT and ERK pathway

4833- Uro,    Unveiling the potential of Urolithin A in Cancer Therapy: Mechanistic Insights to Future Perspectives of Nanomedicine
- Review, Var, NA - Review, AD, NA - Review, IBD, NA
BioAv↝, Urolithin A (UA), a metabolite derived from ellagic acid through gut microbiota metabolism, has emerged as a compelling anticancer agent.
TumAuto↝, UA has multiple mechanisms of action, including the regulation of autophagy, enhancement of mitochondrial function, and inhibition of tumor progression and metastatic pathways.
TumCG↓,
TumMeta↓,
ChemoSen↑, Additionally, its chemo-, immuno-, and radio-sensitization properties further increase its therapeutic advantages
Imm↑,
RadioS↑,
BioAv↑, Nanotechnology-driven approaches, such as nanoparticle formulations, lipids, and powder formulations, have successfully increased the solubility, stability, bioavailability, precise targeted delivery to cancer tissues
other↝, While sparingly soluble in water, UA shows better solubility in organic solvents, such as ethanol and dimethyl sulfoxide.
eff↓, prone to degradation at extreme pH values or high temperatures.
*antiOx↓, UA has gained increasing attention for its pharmacological properties, including anti-oxidant, anti-inflammatory, and anti-cancer activities.
*Inflam↓,
AntiCan↓,
AntiAge↑, UA has potential as a key component in antiaging interventions.
chemoP↑, UA can counteract age-related muscle wasting and enhance physical performance, making it a valuable therapeutic for improving muscle health and combating sarcopenia
*neuroP↑, UA has neuroprotective properties because of its ability to reduce neuroinflammation, improve mitochondrial function, and mitigate oxidative stress,
*ROS↓,
*cognitive↑, suggesting its potential application in neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, and other age-related cognitive disorders)
*lipid-P↓, UA to reduce lipid peroxidation, combat oxidative stress, and improve endothelial function, promoting its role in cardiovascular health
*cardioP↑,
*TNF-α↓, exerts anti-inflammatory effects by suppressing the production of proinflammatory cytokines, such as TNF-α and IL-6, which can be employed for the management of chronic inflammatory conditions (such as rheumatoid arthritis and inflammatory bowel dise
*IL6↓,
GutMicro↑, Given that UA formation and bioactivity are influenced by the gut microbiota, its supplementation could promote a healthier gut microbiome, with potential therapeutic benefits for a wide range of conditions, including irritable bowel syndrome.
TumCCA↑, UA has potent anticancer effects through cell cycle arrest, apoptosis induction, and the modulation of oncogenic signaling pathways.
Apoptosis↑,
angioG↓, regulate the tumor microenvironment by inhibiting angiogenesis and inflammation
NF-kB↓, UA inhibited key signaling pathways, such as the NF-κB and PI3K/AKT pathways, which are critical for tumor progression
PI3K↓,
Akt↓,
Casp↑, UA also promoted apoptosis via the activation of caspases and the downregulation of survival proteins such as Survivin
survivin↓,
TumCP↓, inhibited MCF-7 cell proliferation in vitro and significantly reduced 27-HC-induced tumor growth in vivo.
cycD1/CCND1↓, UA induced cell cycle arrest by downregulating cyclin D1 and c-MYC and promoted apoptosis by increasing the expression of proapoptotic proteins such as Bax while reducing antiapoptotic BCL2 levels.
cMyc↑,
BAX↑,
Bcl-2↓,
COX2↓, UA, a metabolite of pomegranate mesocarp, synergistically reduced COX-2 expression by ~70% and increased cleaved caspase-3 levels
P53↑, UA induces the expression of tumor suppressor proteins such as p53 and p38-MAPK
p38↑,
*ROS↓, UA demonstrates significant antioxidant activity by reducing reactive oxygen species levels and enhancing the activities of key antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase.
*SOD↑,
*GPx↑,
SIRT1↑, UA induced cell cycle arrest and apoptosis while enhancing the expression of key tumor suppressors, including Sirtuin 1 (Sirt1) and Forkhead box protein O1 (FOXO1)
FOXO1↑,
eff↑, UA preferentially accumulates in prostate and intestinal tissues, suggesting its targeted bioactivity.
ChemoSen↑, UA has emerged as a potent chemosensitizing agent that enhances the efficacy of conventional cancer therapies.

4836- Uro,    Urolithin-A Promotes CD8+ T Cell–mediated Cancer Immunosurveillance via FOXO1 Activation
- in-vitro, Var, NA
FOXO1↑, Urolithin-A, a potent mitophagy inducer, emerges as a promising tool to enhance cancer immunosurveillance by activating the FOXO1 transcription factor in CD8+ T cells.
TumCG↓, Preexposure to UroA-enriched Diet is Sufficient to Delay Tumor Growth
PD-1↓, UroA-treated T cells expressed lower level of PD-1 and TIM3
TIM-3↓,


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 ⓘ

ROS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↓, 1,   XIAP↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 3,   Apoptosis↑, 2,   BAX↑, 2,   Bcl-2↓, 2,   Casp↑, 1,   Casp3↑, 2,   Casp8↑, 1,   Casp9↑, 2,   p38↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

other↝, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↝, 1,  

DNA Damage & Repair ⓘ

P53↑, 2,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

FOXO1↑, 4,   GSK‐3β↑, 1,   mTOR↓, 1,   PI3K↓, 2,   TumCG↓, 2,  

Migration ⓘ

TumCP↓, 2,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   Imm↑, 1,   NF-kB↓, 1,   PD-1↓, 1,  

Cellular Microenvironment ⓘ

TIM-3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   BioAv↝, 1,   ChemoSen↑, 2,   Dose↝, 1,   eff↓, 1,   eff↑, 2,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

AntiAge↑, 1,   AntiCan↓, 1,   chemoP↑, 1,   OS↑, 1,   QoL↑, 1,   TumVol↓, 1,  
Total Targets: 50

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   GPx↑, 1,   lipid-P↓, 1,   MDA↓, 1,   ROS↓, 3,   SIRT3↑, 1,   SOD↑, 2,  

Core Metabolism/Glycolysis ⓘ

SIRT1↑, 2,   SREBP2↓, 1,  

Cell Death ⓘ

Apoptosis↓, 1,  

DNA Damage & Repair ⓘ

ATM↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD34↑, 1,   FOXO1↑, 2,   FOXO3↑, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,  

Immune & Inflammatory Signaling ⓘ

IL6↓, 1,   Inflam↓, 1,   TNF-α↓, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   cognitive↑, 1,   neuroP↑, 1,   toxicity∅, 1,  
Total Targets: 23

Scientific Paper Hit Count for: FOXO1, Forkhead box O1
2 Urolithin
1 Alpha-Lipoic-Acid
1 Brucea javanica
1 EGCG (Epigallocatechin Gallate)
1 Propolis -bee glue
1 5-fluorouracil
1 sericin
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#:1164  State#:%  Dir#:2
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