Chrysin / angioG Cancer Research Results

CHr, Chrysin: Click to Expand ⟱
Features:
Chrysin is found in passion flower and honey. It is a flavonoid.
-To reach plasma levels that might more closely match the concentrations used in in vitro studies (typically micromolar), considerably high doses or advanced delivery mechanisms would be necessary.
Chrysin is widely summarized as modulating PI3K/Akt and MAPK pathways in cancer.

Chrysin — Chrysin is a naturally occurring flavone-class flavonoid found in honey, propolis, passionflower, and several plants. Its oncology relevance is mainly preclinical: it shows multi-pathway anticancer activity in cell and animal models, but native oral chrysin has very poor systemic bioavailability and no established approved oncology use.

Primary mechanisms (ranked):

  1. Suppression of PI3K/AKT survival signaling with downstream reduction in proliferation and survival programs.
  2. Induction of mitochondrial apoptosis through Bax/Bcl-2 shift, mitochondrial membrane potential loss, cytochrome c release, and caspase activation.
  3. Context-dependent ROS stress amplification in cancer cells, often linked to mitochondrial injury, ER stress, and apoptosis.
  4. ER stress / unfolded-protein-response activation leading to autophagy or stress-to-death coupling.
  5. Suppression of inflammatory, invasive, angiogenic, and metastatic signaling including NF-κB, MMPs, EMT, VEGF, and HIF-1α axes.
  6. Secondary antioxidant / NRF2-linked cytoprotection in some normal-cell or injury models, which is context-dependent and not necessarily anticancer-selective.

Bioavailability / PK relevance: Native oral chrysin has very poor systemic exposure because of low aqueous solubility, extensive intestinal/hepatic glucuronidation and sulfation, and efflux; human oral bioavailability has been reported as extremely low, often summarized as below 1%. Formulation strategies such as nanoparticles, lipid systems, micelles, cyclodextrins, or structural analogues are commonly proposed for systemic translation.

In-vitro vs systemic exposure relevance: Most anticancer studies use micromolar in-vitro concentrations that are unlikely to be reached in plasma after ordinary oral chrysin. Local intestinal exposure may be more plausible than systemic tumor exposure, but systemic anticancer claims should be treated as formulation-dependent.
LipoMicel may increase bioavailability

Clinical evidence status: Preclinical. Evidence is strong enough for mechanistic oncology interest in cell and animal models, including combination/sensitization studies, but there is no mature clinical oncology evidence establishing therapeutic benefit.

-Note half-life 2 hrs, BioAv very poor often <1%
Pathways:
Graphical Pathways

- may induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓
- May Lower AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓ HO1↓
- May Raise AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓,
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMP2↓, MMP9↓, TIMP2, uPA↓, VEGF↓, ROCK1↓, FAK↓, RhoA↓, NF-κB↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓, P53↑, HSP↓,
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, CDK2↓, CDK4↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, FAK↓, ERK↓, EMT↓, TOP1↓, TET1↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, cMyc↓, GLUT1↓, LDH↓, HK2↓, PDKs↓, HK2↓, GRP78↑, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, Notch↓, PDGF↓, EGFR↓,
- Others: PI3K↓, AKT↓, STAT↓, Wnt↓, AMPK↓, ERK↓, JNK, TrxR,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Chrysin Mechanistic Profile

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 PI3K AKT survival signaling PI3K↓; AKT phosphorylation↓; survival signaling↓ ↔ R, G Growth and survival suppression Central hub mechanism reported across multiple tumor models; also supports chemosensitization.
2 Mitochondrial apoptosis MMP↓; Bax↑; Bcl-2↓; cytochrome c↑; caspase-9/3↑ ↔ or lower sensitivity R, G Intrinsic apoptosis execution One of the most consistent anticancer endpoints, usually downstream of stress and survival-pathway suppression.
3 Mitochondrial ROS stress ROS↑ (context-dependent); oxidative stress↑; lipid peroxidation↑ ROS↓ or antioxidant protection (context-dependent) P, R, G Stress amplification Direction is dose- and model-dependent; cancer models often show pro-oxidant stress, while normal injury models may show antioxidant behavior.
4 ER stress and UPR ER stress↑; GRP78↑; UPR↑; autophagy or apoptosis↑ ↔ R, G Stress-to-death coupling Important in several chrysin cancer models and in some drug-combination effects.
5 NF-κB inflammatory transcription NF-κB↓; COX-2↓; IL-6↓; TNF-α↓ Inflammatory injury signaling↓ R, G Anti-inflammatory and anti-survival signaling May contribute to reduced proliferation, invasion, and cytokine-driven tumor support.
6 Invasion EMT and MMPs EMT↓; MMP-2↓; MMP-9↓; uPA↓; migration↓; invasion↓ ↔ G Anti-invasive phenotype Mechanistically relevant for metastasis models but generally later and context-dependent.
7 Angiogenesis and HIF-1α VEGF signaling HIF-1α↓; VEGF↓; angiogenic output↓ ↔ G Anti-angiogenic support Reported in preclinical models; may overlap with oxidative stress and DNA damage response pathways.
8 Glycolysis and metabolic stress GLUT1↓; HK2↓; LDH↓; PDK1↓; lactate production↓; ATP↓ ↔ G Metabolic suppression Relevant but less central than apoptosis and survival signaling; strongest interpretation is model-dependent.
9 NRF2 antioxidant axis NRF2↓ or antioxidant defense↓ (model-dependent) NRF2↑; SOD↑; GSH↑; catalase↑ (context-dependent) R, G Context-dependent redox selectivity Potentially useful but also interpret carefully because NRF2 activation can be protective in normal cells and sometimes undesirable in cancer cells.
10 Chemosensitization and radiosensitization Drug-induced toxicity↑; apoptosis↑; resistance signaling↓ Chemoprotection reported in some injury models G Adjunct sensitization Promising preclinical adjunct signal, but not clinically established.
11 Clinical Translation Constraint Systemic exposure low after native oral dosing Dose and formulation constraints G Translation limitation Very poor oral bioavailability is the dominant practical constraint; formulation or local GI targeting is likely required.

Time-Scale Flag (TSF): P / R / G

  • P: 0–30 min (primary/physical–chemical effects; rapid signaling / phosphorylation shifts)
  • R: 30 min–3 hr (acute stress-response and redox signaling)
  • G: >3 hr (gene-regulatory adaptation and phenotype-level outcomes)
angioG, angiogenesis: Click to Expand ⟱
Source:
Type:
Process through which new blood vessels.
Angiogenesis, the process of new blood vessel formation from pre-existing vessels, plays a crucial role in cancer progression and metastasis. Tumors require a blood supply to grow beyond a certain size and to spread to other parts of the body.
Vascular Endothelial Growth Factor (VEGF): VEGF is one of the most important pro-angiogenic factors. It stimulates endothelial cell proliferation and migration, leading to the formation of new blood vessels. Many tumors overexpress VEGF, which correlates with poor prognosis.
Hypoxia-Inducible Factor (HIF): In response to low oxygen levels (hypoxia), tumors can activate HIF, which in turn promotes the expression of VEGF and other angiogenic factors. This mechanism allows tumors to adapt to their microenvironment and sustain growth.
Scientific Papers found: Click to Expand⟱
2802- CHr,    Chrysin inhibits expression of hypoxia-inducible factor-1alpha through reducing hypoxia-inducible factor-1alpha stability and inhibiting its protein synthesis
- in-vitro, Pca, DU145 - in-vivo, Pca, NA
Hif1a↓, Chrysin inhibited insulin-induced expression of HIF-1alpha by reducing its stability
VEGF↓, Inhibition of HIF-1alpha by chrysin resulted in abrogation of vascular endothelial growth factor expression.
angioG↓, chrysin inhibited DU145 xenograft-induced angiogenesis

6132- CHr,  MET,    Synergistic Growth Inhibitory Effects of Chrysin and Metformin Combination on Breast Cancer Cells through hTERT and Cyclin D1 Suppression
- in-vitro, BC, T47D
eff↑, combination of metformin and chrysin had high synergistic effects in killing cancer cells
cycD1/CCND1↓, significant decrease in cyclin D1 and hTERT gene expression in the T47D breast cancer cell line.
hTERT/TERT↓,
TumCP↓, in vivo studies have revealed that Chrysin suppresses cancer cell proliferation via apoptosis induction, cell cycle alteration, microRNA modulation and inhibition of invasion, metastasis and angiogenesis
Apoptosis↑,
TumCI↓,
TumMeta↓,
angioG↓,
selectivity↑, without triggering undesirable side effects and toxicity to normal cells

6133- CHr,    Chrysin in PI3K/AKT and other apoptosis signalling pathways, and its effect on HeLa cells.
- Review, Var, NA
TumCP↓, chrysin inhibits proliferation, induces apoptosis and reduce angiogenesis in most tested cancer cells, including cervical cancer cells.
Apoptosis↑,
angioG↓,
eff↑, biological activities of chrysin may be improved by modification of the original structure of chrysin or combination therapy.
CYP19↓, Chrysin is also reported as a potent inhibitor of aromatase which is responsible for blocking the conversion of androgen to estrogens
Hif1a↓, Chrysin suppresses HIF-1α/VEGF and angiogenesis
VEGF↓,
NF-kB↓, Chrysin downregulates NFκB and its target genes
PI3K↓, Chrysin inactivates PI3K/AKT signalling pathway in apoptosis
Akt↓,

6135- CHr,    Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative Review
- Review, Var, NA - Review, AD, NA
Inflam↓, various cancers has been demonstrated and it modulates cell signaling pathways, including inflammation, angiogenesis, apoptosis, autophagy, and the cell cycle.
angioG↓,
Apoptosis↑,
TumAuto↑,
TumCCA↑,
BioAv↓, Despite its promising pharmacological activities, the clinical utility of chrysin remains limited due to its poor bioavailability, low solubility, limited permeability, and rapid metabolism.
Half-Life↓,
BioAv↓, The oral bioavailability of chrysin has been reported to range from 0.003% to 0.02%, with a maximum plasma concentration between 12 and 64 nM
*ROS↓, The study reported that chrysin administration protected the kidneys and liver of rats from oxidative damage induced by chronic ethanol consumption
*hepatoP↑, Hepatoprotective Potential
*RenoP↑, The renal protective effect of chrysin was related to increasing the antioxidant enzyme activities and decreasing the regulation of serum renal toxicity markers.
TET1↑, chrysin meaningfully induced the expression of TET1 in GC cells.
MMP9↓, hrysin might contribute to its anticancer effects by regulating MMP-9 expression.
cMyc↓, Both c-Myc and Ki-67 expressions were found to be suppressed in the tumor tissues treated with chrysin and G1-treated tumor tissues
Ki-67↓,
CBR1↓, chrysin directly interacts with CBR1, inhibiting its enzymatic activity at both the molecular and cellular levels.
ROS↑, This inhibition led to elevated intracellular ROS levels, triggering ROS-dependent autophagy
ChemoSen↑, chrysin enhances pancreatic cancer cell sensitivity to gemcitabine by inducing ferroptosis death, both in vitro and in vivo
Bax:Bcl2↑, chrysin increased the Bax/Bcl-2 expression ratio in ATC cells following treatment
PUMA↑, PUMA and Notch-1 were activated, and Slug was inactivated by chrysin treatment
NOTCH1↑,
*AntiDiabetic↑, Anti-Diabetic Potential
*neuroP↑, Neuroprotective Effects
*GABA↑, treatment of chrysin improves levels of GABA, monoamines, glutamic acid, and their metabolites in three brain regions, while also inhibiting DNA fragmentation markers like 8-HdG as well as BDNF.
*DNAdam↓,
*BDNF↑,
*memory↑, protective effects of chrysin against memory impairments associated with hippocampal neurogenesis
*AGEs↓, figure 6
*Aβ↓,
*cardioP↑, Cardioprotective Effects
*AntiArt↑, Anti-Arthritis Potential
eff↑, combination potential was higher than apigenin or chrysin alone.
eff↑, combination of quercetin enhanced the toxic effects of chrysin on the cell lines
*eff↑, neuroprotective synergistic effects of chrysin and kaempferol revealed therapeutic potential in mitigating cerebral ischemi
RadioS↑, study reported that treatment of MDA-MB-231 cells with chrysin in combination with radiation therapy (RT) caused synergistic antitumor properties.
eff↑, the combination of metformin and chrysin demonstrated pronounced synergistic cytotoxic effects on cancer cells
ChemoSen↑, chrysin was combined with a low dose of cisplatin, the resulting growth inhibition was significantly enhanced.
eff↑, demonstrating greater potency than chrysin or silver nanoparticles alone [198].

2785- CHr,    Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
- Review, Var, NA
*NF-kB↓, suppressed pro-inflammatory cytokine expression and histamine release, downregulated nuclear factor kappa B (NF-kB), cyclooxygenase 2 (COX-2), and inducible nitric oxide synthase (iNOS)
*COX2↓,
*iNOS↓,
angioG↓, upregulated apoptotic pathways [28], inhibited angiogenesis [29] and metastasis formation
TOP1↓, suppressed DNA topoisomerases [31] and histone deacetylase [32], downregulated tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β)
HDAC↓,
TNF-α↓,
IL1β↓,
cardioP↑, promoted protective signaling pathways in the heart [34], kidney [35] and brain [8], decreased cholesterol level
RenoP↑,
neuroP↑,
LDL↓,
BioAv↑, bioavailability of chrysin in the oral route of administration was appraised to be 0.003–0.02% [55], the maximum plasma concentration—12–64 nM
eff↑, Chrysin alone and potentially in combination with metformin decreased cyclin D1 and hTERT gene expression in the T47D breast cancer cell line
cycD1/CCND1↓,
hTERT/TERT↓,
MMP-10↓, Chrysin pretreatment inhibited MMP-10 and Akt signaling pathways
Akt↓,
STAT3↓, Chrysin declined hypoxic survival, inhibited activation of STAT3, and reduced VEGF expression in hypoxic cancer cells
VEGF↓,
EGFR↓, chrysin to inhibit EGFR was reported in a breast cancer stem cell model [
Snail↓, chrysin downregulated MMP-10, reduced snail, slug, and vimentin expressions increased E-cadherin expression, and inhibited Akt signaling pathway in TNBC cells, proposing that chrysin possessed a reversal activity on EMT
Slug↓,
Vim↓,
E-cadherin↑,
eff↑, Fabrication of chrysin-attached to silver and gold nanoparticles crossbred reduced graphene oxide nanocomposites led to augmentation of the generation of ROS-induced apoptosis in breast cancer
TET1↑, Chrysin induced augmentation in TET1
ROS↑, Pretreatment with chrysin induced ROS formation, and consecutively, inhibited Akt phosphorylation and mTOR.
mTOR↓,
PPARα↓, Chrysin inhibited mRNA expression of PPARα
ER Stress↑, ROS production by chrysin was the critical mediator behind induction of ER stress, leading to JNK phosphorylation, intracellular Ca2+ release, and activation of the mitochondrial apoptosis pathway
Ca+2↑,
ERK↓, reduced protein expression of p-ERK/ERK
MMP↑, Chrysin pretreatment led to an increase in mitochondrial ROS creation, swelling in isolated mitochondria from hepatocytes, collapse in MMP, and release cytochrome c.
Cyt‑c↑,
Casp3↑, Chrysin could elevate caspase-3 activity in the HCC rats group
HK2↓, chrysin declined HK-2 combined with VDAC-1 on mitochondria
NRF2↓, chrysin inhibited the Nrf2 expression and its downstream genes comprising AKR1B10, HO-1, and MRP5 by quenching ERK and PI3K-Akt pathway
HO-1↓,
MMP2↓, Chrysin pretreatment also downregulated MMP2, MMP9, fibronectin, and snail expression
MMP9↓,
Fibronectin↓,
GRP78/BiP↑, chrysin induced GRP78 overexpression, spliced XBP-1, and eIF2-α phosphorylation
XBP-1↓,
p‑eIF2α↑,
*AST↓, Chrysin administration significantly reduced AST, ALT, ALP, LDH and γGT serum activities
ALAT↓,
ALP↓,
LDH↓,
COX2↑, chrysin attenuated COX-2 and NFkB p65 expression, and Bcl-xL and β-arrestin levels
Bcl-xL↓,
IL6↓, Reduction in IL-6 and TNF-α and augmentation in caspases-9 and 3 were observed due to chrysin supplementation.
PGE2↓, Chrysin induced entire suppression NF-kB, COX-2, PG-E2, iNOS as well.
iNOS↓,
DNAdam↑, Chrysin induced apoptosis of cells by causing DNA fragmentation and increasing the proportions of DU145 and PC-3 cells
UPR↑, Also, it induced ER stress via activation of UPR proteins comprising PERK, eIF2α, and GRP78 in DU145 and PC-3 cells.
Hif1a↓, Chrysin increased the ubiquitination and degradation of HIF-1α by increasing its prolyl hydroxylation
EMT↓, chrysin was effective in HeLa cell by inhibiting EMT and CSLC properties, NF-κBp65, and Twist1 expression
Twist↓,
lipid-P↑, Chrysin disrupted intracellular homeostasis by altering MMP, cytosolic Ca (2+) levels, ROS generation, and lipid peroxidation, which plays a role in the death of choriocarcinoma cells.
CLDN1↓, Chrysin decreased CLDN1 and CLDN11 expression in human lung SCC
PDK1↓, Chrysin alleviated p-Akt and inhibited PDK1 and Akt
IL10↓, Chrysin inhibited cytokines release, TNF-α, IL-1β, IL-10, and IL-6 induced by Ni in A549 cells.
TLR4↓, Chrysin suppressed TLR4 and Myd88 mRNA and protein expression.
NOTCH1↑, Chrysin inhibited tumor growth in ATC both in vitro and in vivo through inducing Notch1
PARP↑, Pretreating cells with chrysin increased cleaved PARP, cleaved caspase-3, and declined cyclin D1, Mcl-1, and XIAP.
Mcl-1↓,
XIAP↓,

2780- CHr,    Anti-cancer Activity of Chrysin in Cancer Therapy: a Systematic Review
- Review, Var, NA
*antiOx↑, antioxidant (13), anti-inflammatory (14), antibacterial (15), anti-hypertensive (16), anti-allergic (17), vasodilator (18),
Inflam↓,
*hepatoP↑, anti-diabetic (19), anti-anxiety (10), anti-viral (20), anti-estrogen (21), liver protective (22), anti-aging (23), anti-seizure (24), and anti-cancer effects (25)
AntiCan↑,
Cyt‑c↑, (1) facilitating the release of cytochrome C from the mitochondria,
Casp3↑, (2) activating caspase-3 and inhibiting the activity of the XIAP molecule,
XIAP↓,
p‑Akt↓, (3) reducing AKT phosphorylation and triggering the PI3K pathway and induction of apoptosis
PI3K↑,
Apoptosis↑,
COX2↓, chrysin interacts weakly with COX-1 binding site whereas displayed a remarkable interaction with COX-2.
FAK↓, ESCC cells: resultant blockage of the FAK/AKT signaling pathways
AMPK↑, A549: activation of AMPK by chrysin contributes to Akt suppression
STAT3↑, 4T1cell: inhibited STAT3 activation
MMP↓, Chrysin induces apoptosis through the intrinsic mitochondrial pathway that disrupts mitochondrial membrane potential (MMP) and increases DNA fragmentation.
DNAdam↑,
BAX↑, produces pro-apoptotic proteins, including Bax and Bak, and activates caspase-9 and caspase-3 in various cancer cells
Bak↑,
Casp9↑,
p38↑, chrysin can inhibit tumor growth by activating P38 MAPK and stopping the cell cycle
MAPK↑,
TumCCA↑,
ChemoSen↑, beneficial in inhibiting chemotherapy resistance of cancer cells
HDAC8↓, chrysin suppresses tumorigenesis by inhibiting histone deacetylase 8 (HDAC8)
Wnt↓, chrysin can attenuate Wnt and NF-κB signaling pathways
NF-kB↓,
angioG↓, chrysin can inhibit angiogenesis and inducing apoptosis in HTh7 cells, 4T1 mice, and MDA-MB-231 cells
BioAv↓, low bioavailability of flavonoids such as chrysin

2781- CHr,  PBG,    Chrysin a promising anticancer agent: recent perspectives
- Review, Var, NA
PI3K↓, It can block Phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) and Mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) signaling in different animals against various cancers
Akt↓,
mTOR↓,
MMP9↑, Chrysin strongly suppresses Matrix metalloproteinase-9 (MMP-9), Urokinase plasminogen activator (uPA) and Vascular endothelial growth factor (VEGF), i.e. factors that can cause cancer
uPA↓,
VEGF↓,
AR↓, Chrysin has the ability to suppress the androgen receptor (AR), a protein necessary for prostate cancer development and metastasis
Casp↑, starts the caspase cascade and blocks protein synthesis to kill lung cancer cells
TumMeta↓, Chrysin significantly decreased lung cancer metastasis i
TumCCA↑, Chrysin induces apoptosis and stops colon cancer cells in the G2/M cell cycle phase
angioG↓, Chrysin prevents tumor growth and cancer spread by blocking blood vessel expansion
BioAv↓, Chrysin’s solubility, accessibility and bioavailability may limit its medical use.
*hepatoP↑, As chrysin reduced oxidative stress and lipid peroxidation in rat liver cells exposed to a toxic chemical agent.
*neuroP↑, Protecting the brain against oxidative stress (GPx) may be aided by increasing levels of antioxidant enzymes such as superoxide dismutase (SOD) and glutathione peroxidase (GPx).
*SOD↑,
*GPx↑,
*ROS↓, A decrease in oxidative stress and an increase in antioxidant capacity may result from chrysin’s anti-inflammatory properties
*Inflam↓,
*Catalase↑, Supplementation with chrysin increased the activity of antioxidant enzymes like SOD and catalase and reduced the levels of oxidative stress markers like malondialdehyde (MDA) in the colon tissue of the rats.
*MDA↓, Antioxidant enzyme activity (SOD, CAT) and oxidative stress marker (MDA) levels were both enhanced by chrysin supplementation in mouse liver tissue
ROS↓, reduction of reactive oxygen species (ROS) and oxidative stress markers in the cancer cells further indicated the antioxidant activity of chrysin
BBB↑, After crossing the blood-brain barrier, it has been shown to accumulate there
Half-Life↓, The half-life of chrysin in rats is predicted to be close to 2 hours.
BioAv↑, Taking chrysin with food may increase the effectiveness of the supplement: increased by a factor of 1.8 when taken with a high-fat meal
ROS↑, In contrast to 5-FU/oxaliplatin, chrysin increases the production of reactive oxygen species (ROS), which in turn causes autophagy by stopping Akt and mTOR from doing their jobs
eff↑, mixture of chrysin and cisplatin caused the SCC-25 and CAL-27 cell lines to make more oxygen free radicals. After treatment with chrysin, cisplatin, or both, the amount of reactive oxygen species (ROS) was found to have gone up.
ROS↑, When reactive oxygen species (ROS) and calcium levels in the cytoplasm rise because of chrysin, OC cells die.
ROS↑, chrysin is the cause of death in both types of prostate cancer cells. It does this by depolarizing mitochondrial membrane potential (MMP), making reactive oxygen species (ROS), and starting lipid peroxidation.
lipid-P↑,
ER Stress↑, when chrysin is present in DU145 and PC-3 cells, the expression of a group of proteins that control ER stress goes up
NOTCH1↑, Chrysin increased the production of Notch 1 and hairy/enhancer of split 1 at the protein and mRNA levels, which stopped cells from dividing
NRF2↓, Not only did chrysin stop Nrf2 and the genes it controls from working, but it also caused MCF-7 breast cancer cells to die via apoptosis.
p‑FAK↓, After 48 hours of treatment with chrysin at amounts between 5 and 15 millimoles, p-FAK and RhoA were greatly lowered
Rho↓,
PCNA↓, Lung histology and immunoblotting studies of PCNA, COX-2, and NF-B showed that adding chrysin stopped the production of these proteins and maintained the balance of cells
COX2↓,
NF-kB↓,
PDK1↓, After the chrysin was injected, the genes PDK1, PDK3, and GLUT1 that are involved in glycolysis had less expression
PDK3↑,
GLUT1↓,
Glycolysis↓, chrysin stops glycolysis
mt-ATP↓, chrysin inhibits complex II and ATPases in the mitochondria of cancer cells
Ki-67↓, the amounts of Ki-67, which is a sign of growth, and c-Myc in the tumor tissues went down
cMyc↓,
ROCK1↓, (ROCK1), transgelin 2 (TAGLN2), and FCH and Mu domain containing endocytic adaptor 2 (FCHO2) were much lower.
TOP1↓, DNA topoisomerases and histone deacetylase were inhibited, along with the synthesis of the pro-inflammatory cytokines tumor necrosis factor alpha (TNF-alpha) and (IL-1 beta), while the activity of protective signaling pathways was increased
TNF-α↓,
IL1β↓,
CycB/CCNB1↓, Chrysin suppressed cyclin B1 and CDK2 production in order to stop cancerous growth.
CDK2↓,
EMT↓, chrysin treatment can also stop EMT
STAT3↓, chrysin block the STAT3 and NF-B pathways, but it also greatly reduced PD-L1 production both in vivo and in vitro.
PD-L1↓,
IL2↑, chrysin increases both the rate of T cell growth and the amount of IL-2

2786- CHr,    Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectives
- Review, Var, NA
Apoptosis↑, chrysin inhibits cancer growth through induction of apoptosis, alteration of cell cycle and inhibition of angiogenesis, invasion and metastasis without causing any toxicity and undesirable side effects to normal cells
TumCCA↑,
angioG↓,
TumCI↓,
TumMeta↑,
*toxicity↓,
selectivity↑,
chemoPv↑, Induction of phase II detoxification enzymes, such as glutathione S-transferase (GST) or NAD(P)H:quinone oxidoreductase (QR) is one of the major mechanism of protection against initiation of carcinogenesis
*GSTs↑,
*NADPH↑,
*GSH↑, upregulation of antioxidant and carcinogen detoxification enzymes (glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR), GST and QR)
HDAC8↓, inhibits of HDAC8 enzymatic activity
Hif1a↓, Prostate DU145: Inhibits HIF-1a expression through Akt signaling and abrogation of VEGF expression
*ROS↓, chrysin (20 and 40 mg/kg) was shown to exhibit chemopreventive activity by ameliorating oxidative stress and inflammation via NF-kB pathway
*NF-kB↓,
SCF↓, Chrysin has also been reported to have the ability to abolish the stem cell factor (SCF)/c-Kit signaling in human myeloid leukemia cells by preventing the PI3 K pathway
cl‑PARP↑, (PARP) and caspase-3 and concurrently decreasing pro-survival proteins survivin and XIAP
survivin↓,
XIAP↓,
Casp3↑, activation of caspase-3 and -9.
Casp9↑,
GSH↓, chrysin sustains a significant depletion of intracellular GSH concentrations in human NSCLC cells
ChemoSen↑, chrysin potentiates cisplatin toxicity, in part, via synergizing pro-oxidant effects of cisplatin by inducing mitochondrial dysfunction, and by depleting cellular GSH, an important antioxidant defense
Fenton↑, ability to participate in a fenton type chemical reaction
P21↑, upregulation of p21 independent of p53 status and decrease in cyclin D1, CDK2 protein levels
P53↑,
cycD1/CCND1↓,
CDK2↓,
STAT3↓, chrysin inhibits angiogenesis through inhibition of STAT3 and VEGF release mediated by hypoxia through Akt signaling pathway
VEGF↓,
Akt↓,
NRF2↓, Chrysin treatment significantly reduced nrf2 expression in cells at both the mRNA and protein levels through down-regulation of PI3K-Akt and ERK pathways.

2787- CHr,    Network pharmacology unveils the intricate molecular landscape of Chrysin in breast cancer therapeutics
- Analysis, Var, MCF-7
TumCP↓, implicated in cell proliferation, angiogenesis, invasion, and metastasis
angioG↓,
TumCI↓,
TumMeta↓,
TP53↑, Chrysin exhibited strong binding interactions with several key hub proteins, notably TP53, AKT1, and CASP3, suggesting its capacity to inhibit tumorigenesis in breast cancer
Akt↓,
Casp3↑,
tumCV↓, dose-dependent reduction in cell viability was observed, with an IC50 value of 67.43 and 22.55 µM for 24 and 48 h
TNF-α↓, chrysin binds strongly to TNF-α, potentially inhibiting its function.
BioAv↑, Improved bioavailability of chrysin via its interaction with HSA could enhance its therapeutic efficacy, a factor that could be further explored in future pharmacokinetic studies
BioAv↑, Albumin’s ability to bind and transport Chrysin could influence the bioavailability of the flavonoid, potentially enhancing its therapeutic effects.
AKT1↓, chrysin effectively inhibits AKT1,

2788- CHr,    Chrysin: Sources, beneficial pharmacological activities, and molecular mechanism of action
- Review, Var, NA
*neuroP↑, Chrysin mitigates neurotoxicity, neuroinflammation, and oxidative stress.
*Inflam↓,
*ROS↓,
NF-kB↓, Chrysin treatment maintains the antioxidant armory and suppresses the activation of redox-active transcription factor NF-kB
*PCNA↓, Chrysin supplementation downregulated the expression of PCNA, COX-2, and NF-kB
*COX2↓,
ChemoSen↑, Chrysin is effective in attenuating cisplatin-induced expression of both COX-2 and iNOS
Hif1a↓, DU145: Chrysin suppressed the expression of HIF-1a of tumor cells in vitro and inhibited tumor cell-induced angiogenesis in vivo
angioG↓,
*chemoPv↑, Chrysin as an effective chemopreventive agent having the capability to obstruct DEN initiated and Fe-NTA promoted renal cancer in the rat model
PDGF↓, Chrysin functionally suppresses PDGF-induced proliferation and migration in VSMCs
*memory↑, Chrysin is effective in attenuating memory impairment, oxidative stress, acting as an antiaging agent
*RenoP↑, protected the kidney from damage
*PPARα↑, Chrysin significantly inhibits AGE-RAGE mediated oxidative stress and inflammation through PPAR-g activation
*lipidLev↓, Chrysin was able to decrease plasma lipids concentration because of its antioxidant properties
*hepatoP↑, Chrysin shows promising hepatoprotective and antihyperlipidemic effects, which are evidenced by the decreased levels of triglycerides, free fatty acids, total cholesterol, phospholipids, low-density lipoprotein-C, and very low-density lipoprotein
*cardioP⇅, Chrysin significantly ameliorated myocardial damage
*BioAv↓, despite its therapeutic potential, the bioavailability of chrysin and probably other flavonoids in humans is extremely low, mainly due to poor absorption, rapid metabolism, and rapid systemic elimination.

2797- CHr,    A flavonoid chrysin suppresses hypoxic survival and metastatic growth of mouse breast cancer cells
- in-vivo, BC, NA - in-vitro, BC, 4T1
tumCV↓, Thai propolis extract and chrysin decreased survival of 4T1 cells after exposure to hypoxia (1% O2), for 2 days.
p‑STAT3↓, chrysin inhibited hypoxia-induced STAT3 phosphorylation without affecting HIF-1α protein level.
VEGF↓, Chrysin also abrogated hypoxia-induced VEGF gene
Weight∅, did not affect body weight of the mice
angioG↓, leading to abrogation of hypoxia-induced angiogenesis


Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:


NA, unassigned ⓘ

CBR1↓, 1,  

Redox & Oxidative Stress ⓘ

Fenton↑, 1,   GSH↓, 1,   HO-1↓, 1,   lipid-P↑, 2,   NRF2↓, 3,   ROS↓, 1,   ROS↑, 5,  

Mitochondria & Bioenergetics ⓘ

mt-ATP↓, 1,   MMP↓, 1,   MMP↑, 1,   XIAP↓, 3,  

Core Metabolism/Glycolysis ⓘ

AKT1↓, 1,   ALAT↓, 1,   AMPK↑, 1,   cMyc↓, 2,   Glycolysis↓, 1,   HK2↓, 1,   LDH↓, 1,   LDL↓, 1,   PDK1↓, 2,   PDK3↑, 1,   PPARα↓, 1,  

Cell Death ⓘ

Akt↓, 5,   p‑Akt↓, 1,   Apoptosis↑, 5,   Bak↑, 1,   BAX↑, 1,   Bax:Bcl2↑, 1,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 4,   Casp9↑, 2,   Cyt‑c↑, 2,   hTERT/TERT↓, 2,   iNOS↓, 1,   MAPK↑, 1,   Mcl-1↓, 1,   p38↑, 1,   PUMA↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 2,  

Protein Folding & ER Stress ⓘ

p‑eIF2α↑, 1,   ER Stress↑, 2,   GRP78/BiP↑, 1,   UPR↑, 1,   XBP-1↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 2,   P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,   TP53↑, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 2,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 3,   P21↑, 1,   TumCCA↑, 4,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   ERK↓, 1,   HDAC↓, 1,   HDAC8↓, 2,   mTOR↓, 2,   NOTCH1↑, 3,   PI3K↓, 2,   PI3K↑, 1,   SCF↓, 1,   STAT3↓, 3,   STAT3↑, 1,   p‑STAT3↓, 1,   TOP1↓, 2,   Wnt↓, 1,  

Migration ⓘ

Ca+2↑, 1,   CLDN1↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   p‑FAK↓, 1,   Fibronectin↓, 1,   Ki-67↓, 2,   MMP-10↓, 1,   MMP2↓, 1,   MMP9↓, 2,   MMP9↑, 1,   PDGF↓, 1,   Rho↓, 1,   ROCK1↓, 1,   Slug↓, 1,   Snail↓, 1,   TET1↑, 2,   TumCI↓, 3,   TumCP↓, 3,   TumMeta↓, 3,   TumMeta↑, 1,   Twist↓, 1,   uPA↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 11,   EGFR↓, 1,   Hif1a↓, 5,   VEGF↓, 6,  

Barriers & Transport ⓘ

BBB↑, 1,   GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   COX2↑, 1,   IL10↓, 1,   IL1β↓, 2,   IL2↑, 1,   IL6↓, 1,   Inflam↓, 2,   NF-kB↓, 4,   PD-L1↓, 1,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 3,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,   CYP19↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 4,   BioAv↑, 4,   ChemoSen↑, 5,   eff↑, 9,   Half-Life↓, 2,   RadioS↑, 1,   selectivity↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   AR↓, 1,   EGFR↓, 1,   hTERT/TERT↓, 2,   IL6↓, 1,   Ki-67↓, 2,   LDH↓, 1,   PD-L1↓, 1,   TP53↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   cardioP↑, 1,   chemoPv↑, 1,   neuroP↑, 1,   RenoP↑, 1,   Weight∅, 1,  
Total Targets: 140

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

AntiArt↑, 1,  

Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 1,   GSTs↑, 1,   MDA↓, 1,   ROS↓, 4,   SOD↑, 1,  

Core Metabolism/Glycolysis ⓘ

lipidLev↓, 1,   NADPH↑, 1,   PPARα↑, 1,  

Cell Death ⓘ

iNOS↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↓, 1,   PCNA↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   Inflam↓, 2,   NF-kB↓, 2,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,   GABA↑, 1,  

Protein Aggregation ⓘ

AGEs↓, 1,   Aβ↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   eff↑, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   cardioP↑, 1,   cardioP⇅, 1,   chemoPv↑, 1,   hepatoP↑, 4,   memory↑, 2,   neuroP↑, 3,   RenoP↑, 2,   toxicity↓, 1,  
Total Targets: 34

Scientific Paper Hit Count for: angioG, angiogenesis
11 Chrysin
1 Metformin
1 Propolis -bee glue
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#:61  Target#:447  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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