condition found tbRes List
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.

-Note half-life 2 hrs, BioAv very poor
Pathways:
Graphical Pathways

- induce ROS production
- 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↓, GSH↓ HO1↓
- Raises 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


TumCG, Tumor cell growth: Click to Expand ⟱
Source:
Type:
Normal cells grow and divide in a regulated manner through the cell cycle, which consists of phases (G1, S, G2, and M).
Cancer cells often bypass these regulatory mechanisms, leading to uncontrolled proliferation. This can result from mutations in genes that control the cell cycle, such as oncogenes (which promote cell division) and tumor suppressor genes (which inhibit cell division).
Scientific Papers found: Click to Expand⟱
2793- CHr,    Chrysin Inhibits TAMs-Mediated Autophagy Activation via CDK1/ULK1 Pathway and Reverses TAMs-Mediated Growth-Promoting Effects in Non-Small Cell Lung Cancer
- in-vitro, Lung, A549 - in-vitro, Lung, H157 - in-vivo, NA, NA
TumCG↓, Chrysin displayed a significant inhibitory effect on the growth of NSCLC cells, and it could also suppress the pro-cancer effects of M2-TAMs and inhibit their mediated autophagy
M2 MC↑,
CDK1↓, Chrysin Inhibits Autophagy through the CDK1/ULK1 Pathway

2798- CHr,    Chrysin: a histone deacetylase 8 inhibitor with anticancer activity and a suitable candidate for the standardization of Chinese propolis
- in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
HDAC↓, chrysin is a histone deacetylase inhibitor (HDACi) and that it markedly inhibited HDAC8 enzymatic activity
HDAC8↓,
TumCG↓, chrysin significantly suppressed cell growth and induced differentiation in MDA-MB-231 cells
Diff↑,

2800- CHr,    Chrysin Activates Notch1 Signaling and Suppresses Tumor Growth of Anaplastic Thyroid Carcinoma In vitro and In vivo
- in-vitro, Thyroid, NA
TumCG↓, Oral administration of chrysin suppressed the growth of ATC xenografts by an average of 59% compared with the vehicle control group
NOTCH↑, increase in the active intracellular domain of Notch1 protein
cl‑PARP↑, induction of cleaved Poly ADP-ribose polymerase protein, indicating that the growth inhibition was due to apoptosis.
Apoptosis↑,

2805- CHr,    Chrysin serves as a novel inhibitor of DGKα/FAK interaction to suppress the malignancy of esophageal squamous cell carcinoma (ESCC)
- in-vitro, ESCC, KYSE150 - in-vivo, ESCC, NA
FAK↓, chrysin significantly disrupted the DGKα/FAK signalosome to inhibit FAK-controlled signaling pathways and the malignant progression of ESCC cells both in vitro and in vivo
GlucoseCon↓, Chrysin significantly reduced the levels of glycolytic indexes, such as glucose uptake
Casp3↑, hrysin dose-dependently increased the apoptotic rate and caspase 3/7 activity in KYSE410, KYSE30, and KYSE150 cells.
Casp7↑,
p‑Akt↓, chrysin dose-dependently inhibited the phosphorylation of AKT
TumCG↓, chrysin dose-dependently reduced the growth of ESCC tumors
Weight∅, difference of body weight between chrysin treatment groups and control group is minimal

1033- CHr,    Chrysin inhibits hepatocellular carcinoma progression through suppressing programmed death ligand 1 expression
- vitro+vivo, HCC, NA
TumCG↓,
CD4+↑, enhanced CD4/CD8-
CD8+↑, enhanced CD4/CD8-
PD-L1↓, chrysin significantly down-regulated the expression of PD-L1 in vivo and in vitro


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Results for Effect on Cancer/Diseased Cells:
p‑Akt↓,1,   Apoptosis↑,1,   Casp3↑,1,   Casp7↑,1,   CD4+↑,1,   CD8+↑,1,   CDK1↓,1,   Diff↑,1,   FAK↓,1,   GlucoseCon↓,1,   HDAC↓,1,   HDAC8↓,1,   M2 MC↑,1,   NOTCH↑,1,   cl‑PARP↑,1,   PD-L1↓,1,   TumCG↓,5,   Weight∅,1,  
Total Targets: 18

Results for Effect on Normal Cells:

Total Targets: 0

Scientific Paper Hit Count for: TumCG, Tumor cell growth
5 Chrysin
Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:61  Target#:323  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

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