Chrysin / ChemoSen 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):

Suppression of PI3K/AKT survival signaling with downstream reduction in proliferation and survival programs.
Induction of mitochondrial apoptosis through Bax/Bcl-2 shift, mitochondrial membrane potential loss, cytochrome c release, and caspase activation.
Context-dependent ROS stress amplification in cancer cells, often linked to mitochondrial injury, ER stress, and apoptosis.
ER stress / unfolded-protein-response activation leading to autophagy or stress-to-death coupling.
Suppression of inflammatory, invasive, angiogenic, and metastatic signaling including NF-κB, MMPs, EMT, VEGF, and HIF-1α axes.
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)

ChemoSen, chemo-sensitization: Click to Expand ⟱

Source:

Type:

The effectiveness of chemotherapy by increasing cancer cell sensitivity to the drugs used to treat them, which is known as “chemo-sensitization”.

Chemo-Sensitizers:
-Curcumin
-Resveratrol
-EGCG
-Quercetin
-Genistein
-Berberine
-Piperine: alkaloid from black pepper
-Ginsenosides: active components of ginseng
-Silymarin
-Allicin
-Lycopene
-Ellagic acid
-caffeic acid phenethyl ester
-flavopiridol
-oleandrin
-ursolic acid
-butein
-betulinic acid

Scientific Papers found: Click to Expand⟱

2801-

CHr,

AMP-activated protein kinase (AMPK) activation is involved in chrysin-induced growth inhibition and apoptosis in cultured A549 lung cancer cells

in-vitro,

Lung,

A549

AMPK↑, demonstrated a significant AMPK activation after chrysin treatment in A549 cells
Akt↓, inhibited Akt/mammalian target of rapamycin (mTOR) activation
ChemoSen↑, Chrysin increases doxorubicin-induced AMPK activation to promote A549 cell death and growth inhibition
ROS↑, Recently, studies have confirmed that chrysin is a potent inducer of ROS and in A549 and other cancer cells

2803-

CHr,

5-FU,

Potentiating activities of chrysin in the therapeutic efficacy of 5-fluorouracil in gastric cancer cells

in-vitro,

GC,

AGS

chrysin doses of 40, 50, 60 and 80 µM, and 5-FU doses of 20, 25, 30 and 40 µM,

ChemoSen↑, combination of chrysin and 5-FU significantly increased cytotoxicity more than chrysin or 5-FU alone
TumCCA↑, 5-FU induced apoptosis through p53-p21 activity, while chrysin arrested the cell cycle in the G2/M phase
eff↑, chrysin was co-administered with cisplatin in HepG2 liver cancer cells (19), with docetaxel in A549 non-small cell lung cancer cells (18), and with metformin in breast cancer cells (20), showing synergistic effects
MDR1↓, chrysin inhibits the expression of MDR1

6125-

CHr,

Chrysin enhances anticancer drug-induced toxicity mediated by the reduction of claudin-1 and 11 expression in a spheroid culture model of lung squamous cell carcinoma cells

in-vitro,

SCC,

CLDN1↓, Chrysin, found in high concentration in honey and propolis, decreased CLDN1 and CLDN11 expression in RERF-LC-AI cells derived from human lung SCC.
p‑Akt↓, Taken together, chrysin may bind to Akt and inhibit its phosphorylation, resulting in the elevation of anticancer drug-induced toxicity mediated by reductions in CLDN1 and CLDN11 expression in RERF-LC-AI cells.
ChemoSen↑, We suggest that chrysin may be useful as an adjuvant chemotherapy in lung SCC.

6130-

CHr,

Anticancer Properties of Chrysin on Colon Cancer Cells, In vitro and In vivo with Modulation of Caspase-3, -9, Bax and Sall4

vitro+vivo,

Colon,

CT26

80 μg.mL-1

tumCV↓, chrysin exerted a cytotoxic effect on CT26 cells in a dose dependent manner with IC50= 80 μg.mL-1
Apoptosis↑, chrysin administrated cytotoxicity on colon cancer cells through recruitment of the apoptosis.
TumVol↓, The in vivo assay revealed a remarkable reduction of the colon tumor volume in treated mice (8, 10 mg.kg -1) as compared to the untreated mice.
BAX↑, through down regulation of the sall4 and up-regulation of the Bax.
SALL4↓,
Casp3↑, increase in‏ the caspase-3 and caspase-9 activity in the treated cells‏ in a concentration-dependent manner as compared with‏ the control cells.
Casp9↑,
ChemoSen↑, Recently, a synergism between doxorubicin and chrysin‏ administrated cancer cell death has been shown through‏ chemosensitizing these cells to chemotherapy via GSH‏ depletion in the cancer cells (27).
GSH↓,

6135-

CHr,

Chrysin as a Multifunctional Therapeutic Flavonoid: Emerging Insights in Pathogenesis Management: A Narrative Review

Review,

Var,

Review,

AD,

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].

6136-

CHr,

Tras,

Synergistic anticancer effects of Chrysin and trastuzumab in HER2-Positive breast cancer cells

in-vitro,

BC,

SkBr3

in-vitro,

BC,

BT474

in-vitro,

Nor,

MCF10

eff↑, Chrysin enhanced the anticancer effects of trastuzumab, achieving an optimal combination index (CI) of 0.39 in SKBR3 cells and a similarly strong synergistic profile in BT-474 cells (CI = 0.54).
HER2/EBBR2↓, chrysin also reduced HER2 expression in a significant manner
p‑STAT3↓, combination therapy significantly decreased p-STAT3 and PD-L1 protein levels in SKBR3 and reduced mRNA levels of Tie2 and VEGFR2 in both cell lines.
PD-L1↓,
ChemoSen↑, Chrysin synergistically enhances the efficacy of trastuzumab in HER2-positive SKBR3 and BT-474 breast cancer cells.

2591-

CHr,

doxoR,

Chrysin enhances sensitivity of BEL-7402/ADM cells to doxorubicin by suppressing PI3K/Akt/Nrf2 and ERK/Nrf2 pathway

in-vitro,

HCC,

Bel-7402

NRF2↓, chrysin is a potent Nrf2 inhibitor which sensitizes BEL-7402/ADM cells to ADM
ChemoSen↑, chrysin may be an effective adjuvant sensitizer to reduce anticancer drug resistance by down-regulating Nrf2 signaling pathway.
HO-1↓, Consequently, expression of Nrf2-downstream genes HO-1, AKR1B10, and MRP5 were reduced

2780-

CHr,

Anti-cancer Activity of Chrysin in Cancer Therapy: a Systematic Review

Review,

Var,

*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

2784-

CHr,

Chrysin targets aberrant molecular signatures and pathways in carcinogenesis (Review)

Review,

Var,

Apoptosis↑, apoptosis, disrupting the cell cycle and inhibiting migration without generating toxicity or undesired side‑effects in normal cells
TumCMig↓,
*toxicity↝, toxic at higher doses and the recommended dose for chrysin is <3 g/day
ChemoSen↑, chrysin also inhibits multi‑drug resistant proteins and is effective in combination therapy
*BioAv↓, extremely low bioavailability in humans due to rapid quick metabolism, removal and restricted assimilation. The bioavailability of chrysin when taken orally has been estimated to be between 0.003 to 0.02%
Dose↝, safe and effective in various studies where volunteers have taken oral doses ranging from 300 to 625 mg without experiencing any documented effect
neuroP↑, Chrysin has been shown to exert neuroprotective effects via a variety of mechanisms, such as gamma-aminobutyric acid mimetic properties, monoamine oxidase inhibition, antioxidant, anti-inflammatory and anti-apoptotic activities
*P450↓, Chrysin inhibits cytochrome P450 2E1, alcohol dehydrogenase and xanthine oxidase at various dosages (20 and 40 mg/kg body weight) and protects Wistar rats against oxidative stress
*ROS↓,
*HDL↑, ncreased the levels of high-density lipoprotein cholesterol, glutathione S-transferase, superoxide dismutase and catalase
*GSTs↑,
*SOD↑,
*Catalase↑,
*MAPK↓, inactivate the MAPK/JNK pathway and suppress the NF-κB pathways, and at the same time upregulate the expression of PTEN, and activate the VEGF/AKT pathway
*NF-kB↓,
*PTEN↑,
*VEGF↑,
ROS↑, chrysin treatment in ovarian cancer led to the augmented generation of reactive oxygen species, a decrease in MMP and an increase in cytoplasmic Ca2+,
MMP↓,
Ca+2↑,
selectivity↑, It has been found that chrysin has no cytotoxic effect on normal cells, such as fibroblasts
PCNA↓, Chrysin likewise downregulates proliferating cell nuclear antigen (PCNA) expression in cervical carcinoma cells
Twist↓, Chrysin decreases the expression of TWIST 1 and NF-κB and thus suppresses epithelial-mesenchymal transition (EMT) in HeLa cells
EMT↓,
CDKN1C↑, Chrysin administration led to the upregulation of CDKN1 at the transcript and protein leve
p‑STAT3↑, Chrysin decreased the viability of 4T1 breast cancer cells by suppressing hypoxia-induced phosphorylation of STAT3
MMP2↓, chrysin-loaded PGLA/PEG nanoparticles modulated TIMPS and MMP2 and 9, and PI3K expression in a mouse 4T1 breast tumor model
MMP9↓,
eff↑, Chrysin used alone and as an adjuvant with metformin has been found to downregulate cyclin D and hTERT expression in the breast cancer cell line
cycD1/CCND1↓,
hTERT/TERT↓,
CLDN1↓, CLDN1 and CLDN11 expression have been found to be higher in human lung squamous cell carcinoma. Treatment with chrysin treatment reduces both the mRNA and protein expression of these claudin genes
TumVol↓, Treatment with chrysin treatment (1.3 mg/kg body weight) significantly decreases tumor volume, resulting in a 52.6% increase in mouse survival
OS↑,
COX2↓, Chrysin restores the cellular equilibrium of cells subjected to benzopyrene by downregulating the expression of elevated proteins, such as PCNA, NF-κB and COX-2
eff↑, quercetin and chrysin together decreased the levels of pro-inflammatory molecules, such as IL-6, -1 and -10, and the levels of TNF via the NF-κB pathway.
CDK2↓, Chrysin has been shown to inhibit squamous cell carcinoma via the modulation of Rb and by decreasing the expression of CDK2 and CDK4
CDK4↓,
selectivity↑, chrysin selectively exhibits toxicity and induces the self-programed death of human uveal melanoma cells (M17 and SP6.5) without having any effect on normal cells
TumCCA↑, halting the cell cycle at the G2/M or G1/S phases
E-cadherin↑, upregulation of E-cadherin and the downregulation of cadherin
HK2↓, Chrysin decreased expression of HK-2 in mitochondria, and the interaction between HK-2 and VDAC 2 was disrupted,
HDAC↓, Chrysin, a HDAC inhibitor, caused cytotoxicity, and also inhibited migration and invasion.

2786-

CHr,

Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectives

Review,

Var,

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.

2788-

CHr,

Chrysin: Sources, beneficial pharmacological activities, and molecular mechanism of action

Review,

Var,

*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.

2795-

CHr,

Combination of chrysin and cisplatin promotes the apoptosis of Hep G2 cells by up-regulating p53

in-vitro,

Liver,

HepG2

ChemoSen↑, combination chrysin and cisplatin significantly enhanced the apoptosis of Hep G2 cancer cells
P53↑, chrysin and cisplatin increased the phosphorylation and accumulation of p53 through activating ERK1/2 in Hep G2 cells
ERK↑,
BAX↑, which led to the overexpression of the pro-apoptotic proteins Bax and DR5 and the inhibition of the anti-apoptotic protein Bcl-2.
DR5↑,
Bcl-2↓,
Casp8↑, chrysin and cisplatin promoted both extrinsic apoptosis by activating caspase-8 and intrinsic apoptosis by increasing the release of cytochrome c and activating caspase-9 in Hep G2 cells
Cyt‑c↑,
Casp9↑,

Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

NA, unassigned ⓘ

AntiArt↑, 1,

Redox & Oxidative Stress ⓘ

antiOx↑, 1, Catalase↑, 1, GSH↑, 1, GSTs↑, 2, HDL↑, 1, ROS↓, 4, SOD↑, 1,

Core Metabolism/Glycolysis ⓘ

lipidLev↓, 1, NADPH↑, 1, PPARα↑, 1,

Cell Death ⓘ

MAPK↓, 1,

DNA Damage & Repair ⓘ

DNAdam↓, 1, PCNA↓, 1,

Proliferation, Differentiation & Cell State ⓘ

PTEN↑, 1,

Angiogenesis & Vasculature ⓘ

VEGF↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, Inflam↓, 1, NF-kB↓, 2,

Synaptic & Neurotransmission ⓘ

BDNF↑, 1, GABA↑, 1,

Protein Aggregation ⓘ

AGEs↓, 1, Aβ↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2, eff↑, 1, P450↓, 1,

Functional Outcomes ⓘ

AntiDiabetic↑, 1, cardioP↑, 1, cardioP⇅, 1, chemoPv↑, 1, hepatoP↑, 3, memory↑, 2, neuroP↑, 2, RenoP↑, 2, toxicity↓, 1, toxicity↝, 1,
Total Targets: 36

Scientific Paper Hit Count for: ChemoSen, chemo-sensitization

12 Chrysin
1 5-fluorouracil
1 Trastuzumab
1 doxorubicin

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#:1106  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

Chrysin / ChemoSen Cancer Research Results

Chrysin Mechanistic Profile

Pathway results for Effect on Cancer / Diseased Cells:

NA, unassigned ⓘ

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned ⓘ

Redox & Oxidative Stress ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

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