Luteolin Cancer Research Results

LT, Luteolin: Click to Expand ⟱
Features:
Luteolin a Flavonoid found in celery, parsley, broccoli, onion leaves, carrots, peppers, cabbages, apple skins, and chrysanthemum flowers.
-MDR1 expression, MMP-9, IGF-1 and Epithelial to mesenchymal transition.

Luteolin — a naturally occurring polyhydroxylated flavone (3′,4′,5,7-tetrahydroxyflavone) found in celery, parsley, peppers, broccoli and numerous medicinal plants. It is a dietary phytochemical and experimental small-molecule anticancer/anti-inflammatory agent rather than an approved anticancer drug. Standard abbreviation: LUT or Lut. Luteolin occurs as the free aglycone and as plant glycosides; after oral administration, circulating luteolin is dominated by glucuronide and sulfate conjugates rather than free aglycone. Its cancer pharmacology is pleiotropic and strongly model-dependent, with particularly recurrent effects on PI3K/AKT/mTOR, NF-κB, STAT3, redox regulation, mitochondrial apoptosis, EMT/invasion and cell-cycle control.

Primary mechanisms (ranked):

  1. PI3K/AKT/mTOR survival signaling suppression, reducing proliferation and facilitating apoptosis, autophagy or other programmed cell-death responses.
  2. Redox-selective stress modulation: commonly ↑ ROS in susceptible cancer cells together with ↓ NRF2/HO-1/GSH-associated antioxidant defenses, while frequently reducing oxidative stress and activating protective antioxidant systems in normal tissues.
  3. NF-κB and inflammatory survival signaling inhibition, with context-dependent suppression of TNF-α, IL-6, COX-2 and related inflammatory mediators.
  4. Mitochondrial/intrinsic apoptosis activation through ↓ mitochondrial membrane potential, ↑ BAX:BCL-2 ratio, cytochrome-c release and caspase activation.
  5. STAT3/JAK signaling suppression, reducing survival, stemness, inflammatory signaling and immune-evasion phenotypes in several tumor models.
  6. EMT, migration and invasion suppression through modulation of E-cadherin, N-cadherin, vimentin, MMP2/MMP9, FAK, YAP/TAZ and related pathways.
  7. Cell-cycle arrest through suppression of cyclins/CDKs and context-dependent induction of p21/p27 and p53 signaling.
  8. Metabolic and hypoxic adaptation inhibition, including HIF-1α, PKM2, HK2 and glycolytic signaling in selected models.
  9. Epigenetic modulation, including reported inhibition of DNMTs, HDAC-associated signaling and EZH2 in selected cancer models.
  10. Additional context-dependent cell-death mechanisms including ER stress, autophagy, ferroptosis and pyroptosis.

Bioavailability / PK relevance: Oral luteolin has poor aqueous solubility and unfavorable systemic availability of unconjugated aglycone. It is absorbed from the intestine but undergoes extensive intestinal and hepatic glucuronidation and sulfation. Animal studies report low absolute bioavailability of free luteolin, commonly in the low-single-digit to low-tens percentage range depending on formulation and analytical definition. Nanoemulsions, lipid/phospholipid systems, cyclodextrins, nanoparticles and other delivery systems can substantially improve exposure experimentally. Luteolin and particularly some circulating conjugates can interact with OATP1B1/OATP2B1 transporters; in-vitro CYP inhibition has also been reported, making pharmacokinetic drug interactions plausible at sufficiently high exposure.

In-vitro vs systemic exposure relevance: Many anticancer experiments use approximately 10–100 µM luteolin, often 20–50 µM or higher. These concentrations generally exceed sustained concentrations of free luteolin expected after conventional oral dietary or supplemental dosing because extensive conjugation limits circulating aglycone. Consequently, direct translation of many cell-culture IC50 values to standard oral supplementation is weak. Local gastrointestinal exposure, metabolites, tissue deconjugation and optimized formulations may partly alter this limitation.

Clinical evidence status: Predominantly preclinical, but no longer exclusively preclinical. A 2025 single-arm phase I study administered luteolin 50 mg/day for six months to five men with localized prostate cancer undergoing active surveillance; no treatment-related adverse events were reported, but the study was far too small and uncontrolled to establish anticancer efficacy. A larger phase II single-arm multicenter Japanese study of 50 mg/day for one year is currently recruiting with a planned enrollment of 40 patients. Luteolin is therefore best categorized as early-human/phase I–II investigational evidence, not established cancer therapy. Preclinical evidence for chemotherapy and radiotherapy sensitization is substantial but remains cancer-, drug- and genotype-dependent.


-Note half-life 2–3 hours
BioAv low, but could be improved with Res, or blend of castor oil, kolliphor and polyethylene glycol
Pathways:
- induce ROS production in cancer cell but a few reports of reduction. Always seems to reduce ROS in normal cells.
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMP2↓, MMP9↓, TIMP2, IGF-1↓, VEGF↓, FAK↓, RhoA↓, NF-κB↓, CXCR4↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, DNMT1↓, DNMT3A↓, EZH2↓, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, cMyc↓, LDHA↓, HK2↓, GRP78↑,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓, Integrins↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, β-catenin↓, AMPK, ERK↓, JNK, TrxR**, - Shown to modulate the nuclear translocation of SREBP-2 (related to cholesterol).
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

-"Additionally, when reacted with concentrated sulfuric acid, a zinc salt is produced, resulting in a dark red and yellow solution. These color changes serve as a strong basis for the identification of luteolin"

Common Dietary and Plant Sources of Luteolin

Source Luteolin Content Approximate Equivalent Relative Source Level Notes
Bird chili 1035 mg/kg 103.5 mg/100 g Very high Highest source in the cited quantitative food table; concentration may vary substantially by cultivar, maturity and analytical method.
Belimbi leaves 464.5 mg/kg 46.45 mg/100 g Very high Leaf material; not a common Western dietary source.
Onion leaves 391 mg/kg 39.1 mg/100 g Very high Green onion/scallion-type leaf tissue can contain substantially more luteolin than onion bulbs.
Belimbi fruit 202 mg/kg 20.2 mg/100 g High Tropical fruit source.
Dried asam gelugur 107.5 mg/kg 10.75 mg/100 g High Dried plant material; dry-weight concentration is not directly comparable with fresh vegetables.
Celery 80.5 mg/kg 8.05 mg/100 g High One of the most commonly cited dietary sources of luteolin; content differs among celery varieties and plant parts.
Broccoli 74.5 mg/kg 7.45 mg/100 g High Common dietary source. Other compositional surveys report a broad range, indicating strong cultivar and methodology effects.
Carrot 37.5 mg/kg 3.75 mg/100 g Moderate Common dietary source; luteolin may occur predominantly in glycosylated forms.
Green chili 33 mg/kg 3.3 mg/100 g Moderate Content varies substantially among Capsicum species and cultivars.
Limau purut leaves 30.5 mg/kg 3.05 mg/100 g Moderate Kaffir lime leaves; primarily used as a culinary herb rather than consumed in large quantities.
French bean 11 mg/kg 1.1 mg/100 g Low to moderate Common food source but substantially lower than celery, broccoli or onion leaves in the cited dataset.
White radish 9 mg/kg 0.9 mg/100 g Low Lower-luteolin dietary source in the cited dataset.
Parsley Approximately 19.75 mg/100 g dried Approximately 197.5 mg/kg dried High Frequently cited as a rich luteolin-containing herb. Dry-weight values should not be compared directly with fresh-weight vegetables.
Thyme Approximately 51 mg/100 g Approximately 510 mg/kg Very high Herb source reported in reviews; intake per serving is usually small despite the high concentration.
Peppermint Approximately 11.33 mg/100 g fresh Approximately 113.3 mg/kg High Fresh peppermint is a relatively concentrated herbal source.
Spinach Approximately 1.11 mg/100 g Approximately 11.1 mg/kg Low to moderate Common dietary source but lower than many herbs and celery-family plants.
Cabbage Approximately 0.4–0.6 mg/100 g Approximately 4–6 mg/kg Low Widely consumed but generally a relatively dilute luteolin source.
Black olives Approximately 3.2–17.5 mg/100 g Approximately 32–175 mg/kg Moderate to high Luteolin concentration depends strongly on olive cultivar and processing.
Green olives Approximately 0.2–1.2 mg/100 g Approximately 2–12 mg/kg Low to moderate Generally reported at lower concentrations than black olives.
Apple peel Variable Not consistently quantified Low to moderate Luteolin is reported principally in the peel rather than the flesh; concentration is cultivar-dependent.
Chrysanthemum flowers Variable Not consistently quantified Potentially high Traditional medicinal/tea source containing luteolin and luteolin glycosides.


Luteolin — Cancer Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 PI3K / AKT / mTOR survival signaling ↓ PI3K; ↓ p-AKT; ↓ mTOR ↔ / adaptive modulation R–G ↓ survival and proliferation; ↑ cell death One of the most recurrent anticancer signaling effects; confirmed in multiple tumor systems and newer NSCLC studies.
2 ROS and antioxidant defense ↑ ROS; ↓ SOD/GSH/NRF2/HO-1 (context-dependent) ↓ ROS; ↑ antioxidant defenses (context-dependent) P–R Selective oxidative stress in susceptible tumors Biphasic and highly context-dependent. ROS generation can be mechanistically upstream of NF-κB inhibition, JNK activation, apoptosis and radiosensitization.
3 NRF2 / HO-1 antioxidant survival axis ↓ NRF2; ↓ HO-1 (model-dependent) ↑ NRF2; ↑ HO-1 (model-dependent) R–G ↓ tumor antioxidant capacity and drug resistance Especially relevant in NRF2-high cancer cells. Luteolin has sensitized tumor cells to chemotherapy through NRF2 suppression, whereas NRF2 activation contributes to normal-tissue protection.
4 NF-κB inflammatory survival signaling ↓ NF-κB; ↓ inflammatory survival signaling ↓ pathological NF-κB activation R–G ↑ apoptosis; ↓ inflammation and survival ROS accumulation can participate upstream in some tumor models; not all NF-κB inhibition requires ROS.
5 Mitochondria and intrinsic apoptosis ↓ MMP; ↑ BAX; ↓ BCL-2; ↑ Cyt-c; ↑ caspase-9/3 ↔ / ↓ mitochondrial injury under oxidative-stress conditions R–G ↑ mitochondrial apoptosis A common downstream execution mechanism following AKT inhibition, ROS elevation or ER stress.
6 JAK / STAT3 signaling ↓ STAT3; ↓ p-STAT3 ↔ / ↓ inflammatory STAT3 R–G ↓ proliferation, stemness and immune escape Recent work also links PRDX2 inhibition to JAK2/STAT3 suppression and ↓ PD-L1 in lung adenocarcinoma.
7 EMT and metastatic signaling ↓ EMT; ↑ E-cadherin; ↓ N-cadherin; ↓ vimentin; ↓ MMP2/9 ↔ G ↓ migration, invasion and metastasis PI3K/AKT, TGF-β/Smad, YAP/TAZ, FAK and related axes contribute depending on tumor type.
8 Cell-cycle control ↑ G1 or G2/M arrest; ↓ cyclins/CDKs; ↑ p21/p27 ↔ (model-dependent) G ↓ proliferation Cell-cycle phase varies with tumor lineage and concentration.
9 p53 / JNK apoptotic signaling ↑ JNK; ↑ p53 stability/activity (context-dependent) ↔ R–G ↑ apoptosis and chemotherapy response Cisplatin sensitization can depend strongly on functional p53.
10 Glycolysis and metabolic adaptation ↓ glycolysis; ↓ PKM2; ↓ HK2; ↓ ATP (model-dependent) ↔ G ↓ metabolic support for proliferation Not universal across cancers; strongest evidence comes from selected hepatocellular and other metabolically dependent models.
11 HIF-1α and hypoxic adaptation ↓ HIF-1α; ↓ hypoxic adaptation ↔ G ↓ angiogenesis and hypoxia tolerance Reported in breast, colon and other cancer models; linked to reduced VEGF signaling.
12 VEGF and angiogenesis ↓ VEGF; ↓ VEGFR signaling ↔ / anti-inflammatory vascular effects G ↓ tumor angiogenesis Predominantly preclinical evidence.
13 ER stress and unfolded protein response ↑ PERK/eIF2α/ATF4/CHOP; ↑ ER stress (model-dependent) ↓ pathological ER stress in several injury models R–G ↑ tumor cell death Illustrates luteolin's frequently opposite stress response in malignant versus nonmalignant models.
14 Autophagy ↑ Beclin-1; ↑ LC3-II; ↓ p62 (context-dependent) ↔ / protective modulation G Autophagic stress or contribution to cell death Can be cytotoxic or cytoprotective depending on cancer model and treatment context.
15 GPX4-dependent ferroptosis ↓ GPX4; ↓ GSH; ↑ lipid oxidation; ↑ ferroptosis ↔ / ↓ ferroptotic injury in some normal-tissue models R–G ↑ ferroptotic cancer-cell death Recent colon-cancer work supports GPX4-linked ferroptosis plus enhanced antitumor immune activation.
16 Epigenetic regulation ↓ DNMT activity; ↓ HDAC-associated signaling; ↓ EZH2 (model-dependent) ↔ / context-dependent G Re-expression of growth-suppressive programs Mechanistically interesting but less broadly established than AKT, redox and inflammatory pathways.
17 YAP / Wnt and tumor immunity ↓ YAP; ↓ Wnt-associated signaling; ↓ immune escape ↑ CTL functional activity indirectly G ↑ antitumor T-cell effectiveness 2025 animal work suggests luteolin can enhance tumor-specific CTL therapy; clinical relevance remains unproven.
18 Chemosensitization ↑ response to cisplatin and several other agents (drug-dependent) Variable; possible tissue protection in other contexts G ↓ treatment resistance Mechanisms include ↓ NRF2, ↓ AKT, ↑ p53/JNK, mitochondrial apoptosis and suppression of resistance pathways. Evidence remains predominantly preclinical.
19 Radiosensitization ↑ radiation-induced ROS and apoptosis Potential radioprotection reported in nonmalignant models R–G ↑ radiation response In NSCLC models, p38/ROS/caspase signaling increased radiosensitivity; tumor versus normal-tissue effects require careful context separation.
20 Clinical Translation Constraint High in-vitro concentrations often required Systemic exposure dominated by conjugated metabolites G Limits translation of cell-culture potency Poor aqueous solubility, extensive phase-II metabolism, formulation dependence, possible transporter/drug interactions and extremely limited controlled human oncology evidence remain major constraints.

P: 0–30 min     R: 30 min–3 hr     G: >3 hr



Luteolin — Alzheimer’s disease relevance: Luteolin has substantial preclinical neuroprotective evidence and is sufficiently relevant to Alzheimer’s disease to warrant a separate database section. Reported effects include ↓ amyloid-β production/accumulation, ↓ BACE1-associated amyloidogenic processing, ↓ tau hyperphosphorylation, ↓ neuroinflammation, ↓ oxidative stress, ↓ NLRP3/NF-κB signaling and ↑ BDNF/TrkB-associated neuroplasticity. Acetylcholinesterase inhibition has also been reported. However, evidence remains predominantly cellular and animal; convincing disease-modifying clinical evidence in Alzheimer’s disease is absent. Oral bioavailability and blood-brain exposure of free luteolin remain important translational constraints.

Clinical evidence status: Preclinical. Contemporary reviews identify Alzheimer’s disease as the neurodegenerative disorder in which luteolin has been studied most extensively, but explicitly note that clinical therapeutic evidence remains deficient.

Luteolin — Alzheimer’s Disease Mechanisms

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Neuroinflammation / NF-κB ↓ NF-κB; ↓ IL-1β; ↓ IL-6; ↓ TNF-α ↓ chronic neuroinflammation Among the most consistently proposed neuroprotective actions.
2 Amyloid-β pathology ↓ Aβ; ↓ Aβ42 ↓ amyloid burden Supported predominantly by cellular and animal studies.
3 BACE1 / amyloidogenic processing ↓ BACE1 ↓ amyloidogenic APP processing Potential upstream mechanism contributing to reduced Aβ generation.
4 Tau phosphorylation ↓ p-tau ↓ tau pathology Multiple preclinical models report reduced abnormal tau phosphorylation.
5 Oxidative stress / NRF2 ↓ ROS; ↑ NRF2; ↑ antioxidant defenses ↓ neuronal oxidative injury Direction differs from the pro-oxidant effect frequently exploited in cancer cells.
6 NLRP3 inflammasome ↓ NLRP3 ↓ inflammasome-driven neuronal inflammation Potential bridge between redox stress and neuroinflammation.
7 BDNF / TrkB neuroplasticity ↑ BDNF; ↑ TrkB ↑ synaptic and neuronal support Observed in several neurobehavioral models.
8 Acetylcholinesterase ↓ AChE ↑ cholinergic signaling Primarily biochemical/preclinical evidence; clinical magnitude is unknown.
9 Neuronal apoptosis and mitochondrial stress ↓ apoptosis; ↓ mitochondrial injury ↑ neuronal survival Opposite phenotypic direction from luteolin-induced apoptosis in many cancer models.
10 Clinical Translation Constraint Low free-luteolin exposure; limited human CNS data Uncertain clinical efficacy Human Alzheimer’s disease efficacy trials are insufficient; brain exposure and formulation remain unresolved.


Scientific Papers found: Click to Expand⟱
1539- Api,  LT,    Dietary flavones counteract phorbol 12-myristate 13-acetate-induced SREBP-2 processing in hepatic cells
- in-vitro, Liver, HepG2
SREBP2↓, eff↑, p‑MEK↓, p‑ERK↓,
7815- Api,  LT,  NarG,  QC,  MOR  The role of natural flavonoids on neuroinflammation as a therapeutic target for Alzheimer’s disease: a narrative review
- Review, AD, NA
*NeuroI↓,
2596- Api,  LT,    Natural Nrf2 Inhibitors: A Review of Their Potential for Cancer Treatment
- Review, Var, NA
NRF2↓, chemoPv↑, ChemoSen↑,
2625- Ba,  LT,    Baicalein and luteolin inhibit ischemia/reperfusion-induced ferroptosis in rat cardiomyocyte
- in-vivo, Stroke, NA
*lipid-P↓, *ACSL4∅, *NRF2∅, *GPx4∅, *Ferroptosis↓, *ROS↓, *MDA↓, *eff↑, *HO-1∅,
3633- BBR,  LT,  Cro,  QC,    Naturally Occurring Acetylcholinesterase Inhibitors and Their Potential Use for Alzheimer's Disease Therapy
- Review, AD, NA
*AChE↓, *AChE↓,
8099- KAE,  LT,  CHr,    Kaempherol and Luteolin Decrease Claudin-2 Expression Mediated by Inhibition of STAT3 in Lung Adenocarcinoma A549 Cells
- in-vitro, Lung, A549
CLDN2↓, TumCP↓, STAT3↓,
8370- LT,    Luteolin Induces GPX4-dependent Ferroptosis and Enhances Immune Activation in Colon Cancer
- vitro+vivo, Colon, NA
TumCP↓, ROS↑, Iron↑, lipid-P↑, MDA↑, GSH↓, GPx4↓, Ferroptosis↑, pol-M1↑, CD8+↑, Imm↑,
8368- LT,    A critical role of luteolin-induced reactive oxygen species in blockage of tumor necrosis factor-activated nuclear factor-kappaB pathway and sensitization of apoptosis in lung cancer cells
- in-vitro, Lung, NA
NF-kB↓, ROS↑, JNK↑, Apoptosis↑, SOD↓, eff↓,
8371- LT,    Study on the regulatory mechanism of luteolin inhibiting WDR72 on the proliferation and metastasis of non small cell lung cancer
- vitro+vivo, Lung, A549 - in-vitro, Lung, H1299 - in-vitro, Nor, BEAS-2B
TumCP↓, TumCI↓, TumCMig↓, TumVol↓, p‑Akt↓, Apoptosis↓, EMT↓, Dose↝, Akt↓, WDR72↓, TumMeta↓,
8372- LT,    Luteolin targets peroxiredoxin 2 to augment T-cell-mediated cytotoxicity and suppress lung adenocarcinoma progression
- in-vitro, Lung, NA
TumCP↓, Apoptosis↑, PrxII↓, JAK2↓, STAT3↓, PD-L1↓, Perforin↑, GranB/GZMB↑,
8373- LT,  ATV,    Evaluation of Luteolin Nanosuspensions on Pharmacokinetics of Atorvastatin: Drug-Drug Interactions Using Rat Models
- in-vivo, Nor, NA
*OATPs↓, *cytoP450↓,
8374- LT,  NarG,    Interaction of luteolin, naringenin, and their sulfate and glucuronide conjugates with human serum albumin, cytochrome P450 (CYP2C9, CYP2C19, and CYP3A4) enzymes and organic anion transporting polypeptide (OATP1B1 and OATP2B1) transporters
- in-vitro, Nor, NA
*OATPs↓,
8375- LT,    Luteolin, a flavone ingredient: Anticancer mechanisms, combined medication strategy, pharmacokinetics, clinical trials, and pharmaceutical researches
- Review, Var, NA
TumCP↓, TumCI↓, Apoptosis↑, TumCCA↑, Inflam↓, Ferroptosis↑, Pyro↑, ChemoSen↑, chemoP↑, *BioAv↓, OATPs↓,
8376- LT,  Cisplatin,    Luteolin sensitizes the anticancer effect of cisplatin via c-Jun NH2-terminal kinase-mediated p53 phosphorylation and stabilization
- vitro+vivo, Var, NA
ChemoSen↑, JNK↑, P53↑,
8377- LT,    Luteolin: exploring its therapeutic potential and molecular mechanisms in pulmonary diseases
- Review, Asthma, NA
*PI3K↑, *Akt↑, *Inflam↓, *ROS↓, *BioAv↓, *RenoP↑, *cardioP↑, *neuroP↑, *antiAll↑, *AntiDiabetic↑, *hepatoP↑, *AntiThr↑, *toxicity↓, *IL10↓, *Sepsis↓, *TNF-α↓, *ROS↓, *GSH↑, *Catalase↑, *SOD↑, *MDA↓, *lipid-P↓, *IL4↓, *IL5↓, *PGE2↓, *PI3K↑, *Akt↑, *mTOR↑, *Beclin-1/ATG6↓, *Mucositis↓, *PLA2↓, STAT3↓, PD-L1↓, miR-34a↓, Casp3↑, Casp9↑, Bcl-2↓, BAX↑, Bax:Bcl2↑, Apoptosis↑, ROS↑, EMT↓, E-cadherin↓, DR5↑, LIMK1↓, Pain↓,
8378- LT,    Luteolin and its derivatives: modulation of epithelial-mesenchymal transition in fibrosis and cancer
- Review, Var, NA
EMT↓, TGF-β1↓, Smad1↓, PI3K↓, Akt↓, Hippo↝, YAP/TEAD↓, *NRF2↑, *HO-1↑, *ROS↓, E-cadherin↑, ZO-1↑, Vim↓, CLDN1↓, β-catenin/ZEB1↓, Snail↓, TCF↓, Zeb1↓, angioG↓, eff↑, ROS↑, mtDam↑, MMP↓, ETC↓,
8379- LT,    Luteolin and neuroinflammation: a multi-target therapeutic strategy for central nervous system disorders
- Review, Var, NA - Review, AD, NA - Review, Stroke, NA
*neuroP↑, *Inflam↓, *ROS↓, *Apoptosis↓, *BioAv↓, *BBB∅, Ferroptosis↑, ROS↑, Iron↑, lipid-P↑, MDA↑, GSH↓, GPx4↓, *Aβ↓, *memory↑, *neuroG↑, *NRF2↑, *NLRP3↓, *ROS↓, JAK2↓, STAT3↓, PD-L1↓, Perforin↝, GranB/GZMB↝, hepatoP↑, *Learn↑, *TNF-α↓, *IL1β↓, *IL6↓, *NO↓, *COX2/PTGS2↓, *iNOS↓, *ER Stress↓, *GRP78/BiP↓, *IRE1↓, *cognitive↑, *BAX↓, *Bcl-2↓, *Casp3↓, *PSD95↑, *SNAP25↑, *JNK↓, *eff↑, *mtDam↓, *MMP↑, *Stroke↓, *TJ↑, *MMP9↓, *BBB∅, *NeuroI↓,
8369- LT,    Luteolin inhibits proliferation of lung cancer A549 cells by increasing ROS production and inhibiting the AKT/mTOR signaling pathway and HO-1 expression
- in-vitro, Lung, A549
tumCV↓, TumCP↓, ROS↑, BAX↑, cl‑Casp9↑, Beclin-1/ATG6↑, LC3B-II↑, Bcl-2↓, p62↓, TumAuto↑, p‑Akt↓, p‑mTOR↓, HO-1↓,
8382- LT,    Luteolin as a dietary flavonoid for brain health: modulating neuroinflammation and cognitive decline in neurodegenerative disorders
- Review, AD, NA - Review, Park, NA
*neuroP↑, *Inflam↓, *antiOx↑, *NF-kB↓, *NRF2↑, *BDNF↑, *cognitive↑, *motorD↑, *BBB↑, *BioAv↓, *NO↓, *ROS↓, *NRF2↑, *ARE↑, *MMP↑, *BDNF↑, *Learn↑, *memory↑, *cognitive↑, *p‑JNK↓, *GFAP↓, *AIF1/Iba-1↓, *TNF-α↓, *IL1β↓, *BAX↓, *COX2/PTGS2↓, *BACE/β-secretase↓, *Aβ42↓, *PSD95↑, *SNAP25↑, *lipid-P↓, *GSTs↓, *GSH↑, *SOD↓, *Catalase↓, *AChE↓, *Casp3↓, *Casp9↓,
8367- LT,    Role of Luteolin in Prevention of Oral, Esophageal, Gastric, Pancreatic, and Colon Cancers: Recent Trends and Future Perspectives
- Review, Var, NA
*antiOx↑, ROS↓, Inflam↓, Apoptosis↑,
8366- LT,    Preliminary Evidence on Safety and Clinical Efficacy of Luteolin for Patients With Prostate Cancer Under Active Surveillance
- Trial, Pca, NA
Dose↝, eff↑, SD↑, Ki-67↓, AR↓, NKX3.1↓, miR-29b↑, miR-30a-5p↑,
7825- LT,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*neuroP↑, *OS↑, *antiOx↑, *Aβ42↓, *AChE↓, *Aβ↓, *IRes↓, *p‑tau↓, *ROS↓, *Apoptosis↓, *Inflam↓, *Iron↝,
4883- LT,  CHr,  BRU,  VitC,    An update of Nrf2 activators and inhibitors in cancer prevention/promotion
- Review, Var, NA
*NRF2↓,
4687- LT,  QC,    Dietary Flavonoids Luteolin and Quercetin Suppressed Cancer Stem Cell Properties and Metastatic Potential of Isolated Prostate Cancer Cells
- in-vitro, Pca, DU145
CSCs↓, EMT↓, MMPs↓, TumCMig↓, TumCI↓,
4339- LT,    Luteolin inhibits GPVI-mediated platelet activation, oxidative stress, and thrombosis
- in-vivo, Nor, NA
*AntiAg↑, *ROS↓,
4338- LT,    Luteolin: a natural product with multiple mechanisms for atherosclerosis
- Review, Var, NA
*Inflam↓, *ROS↓, *PDGF↓, *lipid-P↓, *AMPK↑, *SIRT1↑, *AntiAg↑,
4295- LT,    Luteolin Reduces Alzheimer’s Disease Pathologies Induced by Traumatic Brain Injury
- in-vivo, AD, NA
*Aβ↓, *GSK‐3β↓, *p‑tau↓, *BBB↑,
4294- LT,    Luteolin reduces zinc-induced tau phosphorylation at Ser262/356 in an ROS-dependent manner in SH-SY5Y cells
- in-vitro, AD, SH-SY5Y
*tau↓, *antiOx↑,
4293- LT,    Regulatory Role of NF-κB on HDAC2 and Tau Hyperphosphorylation in Diabetic Encephalopathy and the Therapeutic Potential of Luteolin
- in-vivo, Diabetic, NA
*Inflam↓, *antiOx↑, *neuroP↑, *cognitive↑, *p‑mTOR↓, *p‑NF-kB↓, *HDAC2↓, *BDNF↑, *other↓, *p‑tau↓,
8393- LT,    Progress, pharmacokinetics and future perspectives of luteolin modulating signaling pathways to exert anticancer effects: A review
- Review, Var, NA
TumCP↓, TumMeta↓, angioG↓, EMT↓, Imm↝, ChemoSen↑, *Inflam↓, *COX2/PTGS2↓, *NF-kB↓, MMP2↓, MMP9↓, p‑Akt↓, p‑PI3K↓, IGF-2↓, IGF-1R↓, CXCL16↓, NOTCH1↓, HES1↓, VEGF↓, ROS↑,
8406- LT,  Cisplatin,    Luteolin sensitizes the anticancer effect of cisplatin via c-Jun NH2-terminal kinase–mediated p53 phosphorylation and stabilization
- vitro+vivo, Liver, HepG2 - in-vitro, Laryn, HEp2
ChemoSen↑, Dose↝, P53↑,
8405- LT,  Rad,    Luteolin's role as a radiosensitizer by promoting cell death and ROS modulation
- Review, NSCLC, NA
RadioS↑, ROS↑,
8403- LT,    Luteolin induces apoptotic cell death via antioxidant activity in human colon cancer cells
- in-vitro, CRC, HT-29
tumCV↓, selectivity↑, Apoptosis↑, Casp↑, MMP↓, Ca+2↑, BAX↑, Bcl-2↓, Cyt‑c↑, Casp9↑, Casp3↑, ROS↓, SOD↑, Catalase↑, GSH↑, antiOx↑, MAPK↑,
8402- LT,    Luteolin suppresses bladder cancer growth via regulation of mechanistic target of rapamycin pathway
- vitro+vivo, CRC, T24/HTB-9
tumCV↓, TumCCA↑, p‑S6↓, P21↑, Trx1↑, ROS↓, Ki-67↓, mTOR↓, TumCP↓,
8401- LT,    Multi-Faceted Role of Luteolin in Cancer Metastasis: EMT, Angiogenesis, ECM Degradation and Apoptosis
- Review, Var, NA
EMT↓, N-cadherin↓, Vim↓, VEGF↓, VEGFR1↓, MMPs↓, Telomerase↓, NF-kB↓, cMyc↓, Bax:Bcl2↑, Casp3↑, PI3K↓, Akt↓, FOXO3↑, P21↑, p27/CDKN1B↑, cl‑PARP↑, Cyt‑c↑, NOTCH↓, HES1↓, ROS↑, SOD↓, miR-34b-5p↑, Hif1a↓, P21↓, survivin↓, Mcl-1?, Bcl-xL↓, MDM2↓, MMP2↓, MMP9↓, MMP3↓, MMP16↓, miR-384↑, NRF2↓, HO-1↓, angioG↓,
8400- LT,    Luteolin inhibits triple-negative breast cancer by inducing apoptosis and autophagy through SGK1-FOXO3a-BNIP3 signaling
- in-vitro, BC, NA
TumCP↓, TumCI↓, TumCMig↓, Apoptosis↑, SGK1↓, AKT3↓, BNIP3↑,
8399- LT,    Protective effects of luteolin against amyloid beta-induced oxidative stress and mitochondrial impairments through peroxisome proliferator-activated receptor γ-dependent mechanism in Alzheimer's disease
- in-vivo, AD, NA
*memory↑, *cognitive↑, *neuroP↑, *Aβ↓, *mtDam↓, *Apoptosis↓, *PPARγ↑, *ROS↓, *SOD↑, *GSH↑, *NRF2↑, *MFN2↑, *DRP1/DNM1L↓, *FIS1↓, *Bcl-2↑, *BAX↓, *Cyt‑c↓, *cl‑Casp9↓, *cl‑Casp3↓, *IDE↑, *BACE/β-secretase↓, *Aβ42↓,
8398- LT,    Luteolin: Nature's promising warrior against Alzheimer's and Parkinson's disease
- Review, AD, NA - Review, Park, NA
*antiOx↑, *Inflam↓, *AntiBio↑, *AntiCan↑, *hepatoP↑, *neuroP↑, *cardioP↑, *neuroG↑, *BBB↑, *ROS↓, *AChE↓, *p‑T-cadherin↓, *Aβ↓, *memory↑, *TNF-α↓, *IL1β↓, *MCP1/CCL2↓, *RANTES↓, *BioAv↑, *Half-Life↝, *toxicity↓, *BACE/β-secretase↓, *Aβ42↓, *COX2/PTGS2↓, *Bcl-2↓, *Casp3↓, *BAX↓, *GSTs↓, *lipid-P↓, *Casp3↓, *Casp9↓, *memory↑, *GSK‐3β↓, *ChAT↑, *SOD↑, *GPx↑, *MDA↓, *ER Stress↓, *GRP78/BiP↓, *NRF2↑, *motorD↑, *antiAll↑,
8397- LT,    Effects and Mechanisms of Luteolin, a Plant-Based Flavonoid, in the Prevention of Cancers via Modulation of Inflammation and Cell Signaling Molecules
- Review, Var, NA
tumCV↓, TumCP↓, angioG↓, TumCI↓, TumMeta↓, mTOR↓, PI3K↓, Akt↓, STAT3↓, Wnt↓, β-catenin/ZEB1↓, TumCCA↑, Apoptosis↑, hTERT/TERT↓, AP-1↓, NF-kB↓, MAPK↓, HSP90↓, AR↓, IGF-1R↓, Akt↓, NOTCH↓, IL6↓, MMP2↓, MMP3↓, MMP9↓, MMP16↓, TumVol∅, TumW∅, miR-34a↑, miR-107↑, miR-139-5p↑, miR-422a↑, miR-21↓, miR-155↓, miR-224↓, miR-340↓, *toxicity↓,
8396- LT,  Myr,  KAE,  QC,  Api  Antiplatelet Effects of Flavonoid Aglycones Are Mediated by Activation of Cyclic Nucleotide-Dependent Protein Kinases
- in-vivo, Nor, NA
*other↝, *AntiAg↑, *ROS↓,
8395- LT,  PacT,    Luteolin enhances drug chemosensitivity by downregulating the FAK/PI3K/AKT pathway in paclitaxel‑resistant esophageal squamous cell carcinoma
- in-vitro, ESCC, NA
*AntiTum↑, TumCP↓, TumCCA↑, Apoptosis↑, TumCMig↓, EMT↓, ChemoSen↑, PI3K↓, Akt↓, FAK↓,
8394- LT,    Luteolin prevents THP-1 macrophage pyroptosis by suppressing ROS production via Nrf2 activation
- in-vitro, Nor, NA
*Pyro↓, *NLRP3↓, *proCasp1↓, *Casp1↓, *NRF2↑, *HO-1↑, *ROS↓,
8380- LT,    Luteolin, a bioactive compound from Celastrus orbiculatus stem, inhibits cervical cancer via CA2 suppression: A translational study bridging basic research and clinical application
- Trial, Cerv, NA
Dose↝, Ca+2↓,
8392- LT,    Revisiting Luteolin Against the Mediators of Human Metastatic Colorectal Carcinoma: A Biomolecular Approach
- in-vitro, CRC, HCT15 - in-vitro, CRC, HCT116 - in-vitro, CRC, DLD1 - in-vitro, CRC, HT-29 - in-vitro, Nor, RWPE-1
selectivity↑, β-catenin/ZEB1↓, GSK‐3β↑, AKT1↓, PI3K↓, p50↓,
8391- LT,    Mechanism of luteolin against non-small-cell lung cancer: a study based on network pharmacology, molecular docking, molecular dynamics simulation, and in vitro experiments
- in-vitro, NSCLC, NA
other↝, TumCP↓, TumCMig↓, Apoptosis↑, p‑Akt↓, MDM2↓, Bcl-2↓, P53↑, BAX↑,
8390- LT,    Luteolin in Inflammatory Bowel Disease and Colorectal Cancer: A Disease Continuum Perspective
- Review, IBD, NA - Review, CRC, NA
*Diff↝, *Inflam↓, *ROS↓, *GutMicro↑, *IBI↑, TumCP↓, Apoptosis↑, TumCMig↓, TumCI↓, *BioAv↑, *iNOS↓, *TNF-α↓, *IL6↓, *MDA↓, *lipid-P↓, *antiOx↑, *NRF2↑, *HO-1↑, *NQO1↑, *SOD↑, *Catalase↑, *5HT↓, *TPH1↓, *MAPK↓, *ERK↓, *Inflam↓, cycD1/CCND1↓, CDK4↓, TumCCA↑, Casp3↑, Casp9↑, PI3K↓, Akt↓, p‑Akt↓, p‑mTOR↓, E-cadherin↑, N-cadherin↓, Vim↓,
8389- LT,    Luteolin-Manganese Nanozyme Induces Apoptosis and Ferroptosis for Enhanced Cancer Therapy
- in-vitro, Var, NA
ROS↑, Apoptosis↑, cl‑Casp3↑, cl‑Casp9↑, Ferroptosis↑, NRF2↓, GPx4↓, IronCh↑,
8388- LT,    Untargeted metabolomics reveals the mechanisms of luteolin and exercise combination treatment against cognitive impairments in AD mice through modulating autophagy
- in-vivo, AD, NA
*autophagy↝, *cognitive↑,
8387- LT,  QC,  Api,  Ba,    Identification of Flavonoid Compounds in Treating Alzheimer's Disease Based on Network Medicine Framework Strategy
- in-vitro, AD, NA
*neuroP↑, *MMP↑, *Apoptosis↓, *Akt↓, *NF-kB↓, *pol-M2 MC↑, *NeuroI↓,
8386- LT,    Luteolin induces apoptosis in Philadelphia chromosome-positive acute lymphoblastic leukemia cell by regulating the PI3K/AKT signaling pathway
- in-vitro, ALL, SUP-B15
tumCV↓, ROS↑, MMP↓, ATP↓, p‑PI3K↓, p‑Akt↓, p‑STAT3↓, Bcl-2↓, BAX↑, cl‑Casp3↑, cl‑Casp9↑, TumCP↓, eff↓, ChemoSen↑, FAK↓, Synergy↑, BioAv↓, BioAv↑,

Showing Research Papers: 1 to 50 of 106
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* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 106

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   antiOx⇅, 1,   Catalase↓, 3,   Catalase↑, 2,   GPx↓, 1,   GPx4↓, 5,   GSH↓, 8,   GSH↑, 1,   GSR↓, 1,   GSS↑, 1,   GSTs↓, 2,   e-H2O2↓, 1,   i-H2O2∅, 1,   HO-1↓, 8,   HO-1↑, 1,   Iron↑, 3,   lipid-P↑, 2,   MDA↑, 3,   NQO1↓, 2,   NRF2↓, 10,   NRF2↑, 2,   NRF2⇅, 1,   PrxII↓, 1,   ROS↓, 5,   ROS↑, 23,   SOD↓, 8,   SOD↑, 1,   SOD2↓, 1,   Trx1↑, 2,   TrxR1↓, 1,   VitC↓, 1,   VitE↓, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 2,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC2↓, 3,   compI↓, 1,   compIII↓, 1,   compV↓, 1,   ETC↓, 2,   mtDam↑, 3,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT∅, 1,   ATP↓, 2,   FASN↓, 2,   Glycolysis↓, 2,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   p‑GSK‐3β↓, 1,   HK1↓, 1,   HK2↓, 1,   PKM2↓, 1,   p‑S6↓, 1,   SIRT1↓, 2,   SREBP2↓, 1,  

Cell Death(tgid=5) ⓘ

AIF↑, 1,   APAF1↑, 1,   Apoptosis↓, 2,   Apoptosis↑, 25,   ASC↓, 1,   BAD↑, 1,   BAX↑, 14,   Bax:Bcl2↑, 3,   Bcl-2↓, 14,   Bcl-xL↓, 3,   BID↑, 1,   BNIP3↑, 2,   BOK↑, 1,   Casp↑, 2,   Casp1↓, 1,   Casp12↑, 2,   cl‑Casp12↑, 1,   cl‑Casp12↝, 1,   Casp3↑, 11,   cl‑Casp3↑, 4,   Casp7↑, 1,   Casp8↑, 3,   cl‑Casp8↑, 1,   Casp9↑, 8,   cl‑Casp9↑, 4,   proCasp9↓, 1,   Cyt‑c↑, 7,   DR5↑, 6,   FADD↑, 1,   Fas↑, 4,   FasL↑, 1,   Ferroptosis↑, 6,   GranB/GZMB↑, 1,   GranB/GZMB↝, 1,   GSDMD↑, 1,   iNOS↓, 1,   Mcl-1?, 1,   Mcl-1↓, 2,   MDM2↓, 4,   p‑MDM2↓, 1,   NAIP↓, 1,   necrosis↑, 1,   p38↑, 1,   p‑p38↑, 2,   Perforin↑, 1,   Perforin↝, 1,   Pyro↑, 2,   survivin↓, 3,   TumCD↑, 1,   XIAP↓, 4,   YAP/TEAD↓, 3,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 12,   Akt↑, 1,   p‑Akt↓, 8,   AKT1↓, 3,   Akt2↓, 1,   AKT3↓, 1,   cMET↓, 1,   EGFR↓, 1,   EGFR↑, 1,   p‑EGFR↓, 1,   ERK↓, 2,   ERK↑, 1,   p‑ERK↓, 3,   HER2/EBBR2↓, 1,   HGF/c-Met↓, 2,   Hippo↝, 1,   IGF-1R↓, 2,   IKKα↓, 1,   JAK2↓, 2,   JNK↓, 1,   JNK↑, 4,   p‑JNK↑, 1,   LIMK1↓, 1,   p‑MAP2K1/MEK1↓, 1,   MAPK↓, 4,   MAPK↑, 2,   p‑MAPK↓, 1,   p‑MEK↓, 1,   mTOR↓, 4,   p‑mTOR↓, 2,   PI3K↓, 11,   p‑PI3K↓, 3,   PKCδ↓, 1,   PTEN↓, 1,   RAS↓, 1,   SGK1↓, 1,   p‑Src↓, 1,   STAT3↓, 8,   p‑STAT3↓, 5,   p‑STAT6↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

ATF2↓, 1,   ATF4↑, 2,   p‑ATF4↝, 1,   cMyc↓, 4,   p‑cMyc↑, 1,   DNMT1↓, 2,   DNMT3A↓, 1,   DNMTs↓, 2,   EZH2↓, 2,   FOXO1↓, 1,   FOXO3↑, 1,   H3↓, 1,   ac‑H3↓, 1,   H4↓, 1,   ac‑H4↓, 1,   HATs↓, 1,   HDAC↓, 4,   HES1↓, 2,   miR-107↑, 2,   miR-139-5p↑, 2,   miR-155↓, 2,   miR-21↓, 2,   miR-224↓, 2,   miR-29b↑, 1,   miR-30a-5p↑, 1,   miR-340↓, 2,   miR-34a↓, 1,   miR-34a↑, 2,   miR-34b-5p↑, 1,   miR-384↑, 2,   miR-422a↑, 2,   Myc↓, 1,   other↝, 1,   SD↑, 1,   SOX4↓, 1,   TET3↑, 1,   tumCV↓, 7,  

Protein Folding & ER Stress(tgid=8) ⓘ

cl‑ATF6↑, 1,   CHOP/DDIT3↑, 3,   p‑CHOP/DDIT3↝, 1,   eIF2α↑, 2,   p‑eIF2α↑, 2,   p‑eIF2α↝, 1,   ER Stress↑, 5,   GRP78/BiP↑, 1,   GRP94↑, 1,   HSP90↓, 3,   PERK↑, 2,   p‑PERK↝, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1/ATG6↑, 5,   LC3B-II↑, 2,   LC3II↑, 3,   p62↓, 1,   TumAuto↑, 5,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   DNArepair↓, 1,   ERCC3↑, 1,   hTERT/TERT↓, 4,   NKX3.1↓, 1,   P53↑, 8,   PARP↑, 1,   cl‑PARP↑, 2,   PCNA↓, 2,   Telomerase↓, 3,   TOP1↓, 1,   TOP2↓, 1,   XRCC1↓, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 5,   CDK4↓, 3,   CDK6↓, 1,   p‑CHK1↑, 1,   cycA1/CCNA1↑, 1,   CycB/CCNB1↓, 3,   cycD1/CCND1↓, 4,   cycE/CCNE↓, 1,   Ki-67↓, 4,   P21↓, 1,   P21↑, 5,   p27/CDKN1B↑, 2,   TumCCA↑, 15,  

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

ALDH1A1↓, 1,   CD34↓, 1,   cFos↑, 1,   CSCs↓, 2,   GDF15↓, 1,   IGF-1↓, 1,   IGF-2↓, 1,   Ki-67↓, 4,   MSCmark↓, 1,   NICD↓, 1,   NOTCH↓, 4,   NOTCH1↓, 3,   TAZ↓, 2,   TumCG↓, 5,   TumCP?, 1,   TumCP↓, 24,   WDR72↓, 1,   Wnt↓, 4,  

Migration(tgid=13) ⓘ

AEG1↓, 1,   AP-1↓, 1,   AXL↓, 1,   Ca+2↓, 1,   Ca+2↑, 3,   Cdc42↓, 1,   E-cadherin↓, 2,   E-cadherin↑, 8,   EM↑, 1,   EMT↓, 13,   FAK↓, 5,   ITGA6↓, 1,   ITGB1↓, 1,   MET↓, 1,   p‑MET↓, 1,   MMP1↓, 1,   MMP16↓, 3,   MMP2↓, 8,   MMP3↓, 3,   MMP9↓, 8,   MMPs↓, 2,   N-cadherin↓, 8,   PDGF↓, 1,   Rac1↓, 1,   Rho↓, 1,   Smad1↓, 1,   Snail↓, 4,   TET1↑, 2,   TGF-β↓, 1,   TGF-β1↓, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TumCA↓, 1,   TumCI↓, 8,   TumCMig↓, 11,   TumMeta↓, 5,   Twist↓, 2,   Tyro3↓, 1,   Vim↓, 7,   Vim↑, 1,   Zeb1↓, 1,   β-catenin/ZEB1↓, 6,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 8,   ECM/TCF↓, 1,   HIF-1↓, 1,   Hif1a↓, 3,   VEGF↓, 6,   VEGFR1↓, 1,   VEGFR2/KDR/Flk1↓, 2,  

Barriers & Transport(tgid=15) ⓘ

CLDN1↓, 2,   CLDN2↓, 1,   MMP↓, 8,   OATPs↓, 1,   ZO-1↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD8+↑, 1,   COX2/PTGS2↓, 1,   CXCL16↓, 1,   CXCR4↓, 1,   HMGB1↓, 1,   ICAM-1↓, 1,   IFN-γ↓, 1,   IL1↓, 1,   IL18↓, 1,   IL1β↓, 1,   IL2↓, 1,   IL2↑, 1,   IL6↓, 4,   IL8↓, 1,   Imm↑, 1,   Imm↝, 1,   Inflam↓, 2,   pol-M1↑, 1,   NF-kB↓, 12,   p‑NF-kB↑, 1,   NLRP3↓, 1,   NLRP3↑, 1,   p50↓, 1,   p‑p65↓, 1,   PD-1↓, 1,   PD-L1↓, 4,   TCF↓, 1,   TNF-α↓, 3,  

Synaptic & Neurotransmission(tgid=18) ⓘ

PTN↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

AR↓, 4,   CYP19↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 2,   BioAv↑, 4,   BioAv↝, 1,   ChemoSen↓, 1,   ChemoSen↑, 15,   CYP1A1↓, 2,   CYP1A2↓, 1,   Dose?, 1,   Dose↝, 5,   eff↓, 6,   eff↑, 6,   Half-Life↝, 1,   MDR1↓, 2,   P450↓, 1,   RadioS↑, 4,   selectivity↑, 4,   Synergy↑, 2,   TET2↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT∅, 1,   AR↓, 4,   AST∅, 1,   CEA↓, 1,   EGFR↓, 1,   EGFR↑, 1,   p‑EGFR↓, 1,   EZH2↓, 2,   HER2/EBBR2↓, 1,   hTERT/TERT↓, 4,   IL6↓, 4,   Myc↓, 1,   NSE↓, 1,   PD-L1↓, 4,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 2,   cachexia↓, 1,   cardioP↑, 1,   chemoP↑, 4,   chemoPv↑, 1,   hepatoP↑, 1,   Pain↓, 1,   TumVol↓, 1,   TumVol∅, 1,   TumW∅, 1,   Weight∅, 1,  

Infection & Microbiome(tgid=24) ⓘ

GutMicro↑, 1,  
Total Targets: 371

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 15,   ARE↑, 1,   Catalase↓, 1,   Catalase↑, 7,   GPx↑, 3,   GPx4∅, 1,   GSH↑, 8,   GSR↑, 2,   GSTs↓, 2,   GSTs↑, 2,   HO-1↑, 6,   HO-1∅, 1,   Iron↝, 1,   lipid-P↓, 9,   MDA↓, 5,   MDA↑, 1,   NQO1↑, 2,   NRF2↓, 2,   NRF2↑, 12,   NRF2∅, 1,   PrxII↑, 1,   ROS↓, 28,   SOD↓, 1,   SOD↑, 12,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

DRP1/DNM1L↓, 1,   FIS1↓, 1,   MFN2↑, 1,   mtDam↓, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

ACSL4∅, 1,   ALAT↓, 1,   AMPK↑, 2,   ATP↑, 2,   cytoP450↓, 1,   GSK‐3β↓, 3,   LDHA↑, 1,   PLA2↓, 1,   SIRT1↑, 2,   SREBP1/SREBF1↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 6,   BAX↓, 5,   Bax:Bcl2↓, 1,   Bcl-2↓, 2,   Bcl-2↑, 2,   Casp1↓, 2,   proCasp1↓, 1,   Casp3↓, 8,   cl‑Casp3↓, 1,   Casp9↓, 3,   Casp9↑, 1,   cl‑Casp9↓, 1,   Cyt‑c↓, 2,   Ferroptosis↓, 1,   iNOS↓, 3,   p‑p38↓, 1,   Pyro↓, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Akt↓, 1,   Akt↑, 3,   p‑Akt↓, 1,   CREB↑, 1,   ERK↓, 1,   p‑ERK↓, 1,   JNK↓, 1,   p‑JNK↓, 2,   MAPK↓, 1,   p‑MEK↓, 1,   p‑MKK4↑, 1,   mTOR↑, 2,   p‑mTOR↓, 1,   PI3K↓, 1,   PI3K↑, 3,   Raf↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

AntiThr↑, 1,   ATF4↓, 1,   HDAC2↓, 1,   other↓, 2,   other↝, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP/DDIT3↓, 1,   ER Stress↓, 4,   GRP78/BiP↓, 2,   GRP78/BiP↑, 1,   IRE1↓, 1,   UPR↑, 1,  

Autophagy & Lysosomes(tgid=9) ⓘ

autophagy↝, 1,   Beclin-1/ATG6↓, 3,  

DNA Damage & Repair(tgid=10) ⓘ

p‑γH2AX↓, 1,  

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

Diff↝, 1,   neuroG↑, 3,  

Migration(tgid=13) ⓘ

AntiAg↑, 3,   AP-1↓, 1,   E-cadherin↑, 1,   MMP1↓, 1,   MMP9↓, 1,   PDGF↓, 1,   p‑T-cadherin↓, 1,   TregCell↑, 1,   TXNIP↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

NO↓, 3,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 5,   BBB∅, 2,   IBI↑, 1,   MMP↑, 5,   OATPs↓, 2,   TJ↑, 1,   ZO-1↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

AIF1/Iba-1↓, 1,   COX2/PTGS2↓, 6,   COX2/PTGS2∅, 1,   IFN-γ↓, 1,   IL10↓, 1,   IL10↑, 1,   IL18↓, 1,   IL1β↓, 6,   IL2↓, 1,   IL33↓, 1,   IL4↓, 1,   IL5↓, 1,   IL6↓, 5,   IL8↓, 1,   Inflam↓, 14,   pol-M2 MC↑, 1,   MCP1/CCL2↓, 1,   NeuroI↓, 3,   NF-kB↓, 5,   p‑NF-kB↓, 1,   NLRP3↓, 3,   PGE2↓, 2,   RANTES↓, 1,   TLR4↓, 1,   TNF-α↓, 7,  

Cellular Microenvironment(tgid=17) ⓘ

GFAP↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

5HT↓, 1,   AChE↓, 6,   BDNF↑, 6,   ChAT↑, 1,   PSD95↑, 3,   SNAP25↑, 2,   TPH1↓, 1,   TrkB↑, 2,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 7,   Aβ42↓, 4,   BACE/β-secretase↓, 4,   IDE↑, 1,   tau↓, 2,   p‑tau↓, 3,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

PPARα↑, 1,   PPARγ↑, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 7,   BioAv↑, 3,   BioAv↝, 1,   eff↑, 4,   GSTA1↑, 2,   Half-Life↝, 2,   Synergy↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1,   AST↓, 1,   BloodF↑, 1,   IL6↓, 5,   IRes↓, 1,  

Functional Outcomes(tgid=23) ⓘ

antiAll↑, 3,   AntiCan↑, 1,   AntiDiabetic↑, 1,   AntiTum↑, 1,   cardioP↑, 3,   cognitive↑, 7,   hepatoP↑, 3,   Learn↑, 2,   memory↑, 6,   Mood↑, 2,   motorD↑, 2,   Mucositis↓, 2,   neuroP↑, 12,   OS↑, 1,   RenoP↑, 2,   Stroke↓, 1,   toxicity↓, 4,   toxicity↑, 1,  

Infection & Microbiome(tgid=24) ⓘ

AntiBio↑, 1,   GutMicro↑, 2,   Sepsis↓, 1,  
Total Targets: 181

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#:118  Target#:%  State#:%  Dir#:%
  wNotes=0  sortOrder:rid,rpid

 

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