Chrysin / Vim 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.

-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

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 PI3K → AKT (± mTOR) survival axis ↓ PI3K/AKT (often ↓ p-AKT; downstream growth signals ↓) ↔ R, G Growth/survival suppression Frequently reported hub effect; contributes to reduced proliferation and sensitization to stress/apoptosis programs.
2 Intrinsic apoptosis (p53/Bcl-2 family → caspase-9/3) ↑ p53 axis (context); Bax↑/Bcl-2↓; ↑ caspase-9/3; apoptosis ↑ ↔ (generally less activation) G Apoptosis execution Common endpoint across many tumor models; often downstream of survival-pathway suppression and stress signaling.
3 ER stress / UPR (PERK and related arms) ER stress ↑; UPR activation ↑ ↔ R, G Stress-to-death coupling ER stress has been directly shown in chrysin-treated cancer cells and can couple to apoptosis.
4 JAK / STAT3 signaling ↓ STAT3 signaling (context) ↔ R, G Anti-survival transcription STAT3 inhibition is reported in cancer models and often aligns with reduced proliferation and increased apoptosis.
5 ROS / oxidative stress (context-dependent) ROS modulation (often ↑ mitochondrial ROS in tumor models) ↔ / antioxidant behavior in some contexts P, R, G Stress amplifier (variable) Direction depends on dose/model; avoid absolute “ROS always ↑/↓”. Oxidative stress + DDR has been linked to anti-angiogenic effects in vivo in melanoma models.
6 MAPK re-wiring (ERK / JNK / p38) MAPK shifts; JNK/p38 often stress-activated; ERK variable ↔ P, R, G Signal reprogramming MAPK effects differ by cell line; chrysin can suppress JNK/ERK signaling to reduce MMP-9 in some models.
7 Cell-cycle arrest / proliferation control Cell-cycle arrest ↑; proliferation ↓ ↔ G Cytostasis Often observed as later phenotype-level outcomes, downstream of signaling changes.
8 Invasion / metastasis (MMP-9; EMT programs) MMP-9 ↓; migration/invasion ↓ (context) ↔ G Anti-invasive phenotype Chrysin can reduce MMP-9 expression via AP-1 suppression and MAPK pathway effects in certain cancer models.
9 Angiogenesis (VEGF/angiogenic outputs) Angiogenesis outputs ↓ (context) ↔ G Anti-angiogenic support In melanoma models, chrysin has been associated with angiogenesis regression linked to oxidative stress and DNA damage response.
10 Bioavailability constraint (oral PK limitation) Systemic exposure often low without formulation — — Translation constraint Native chrysin oral bioavailability is extremely low due to poor solubility and extensive glucuronidation/sulfation with efflux; formulation strategies are commonly required for systemic effects.

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)
Vim, Vimentin: Click to Expand ⟱
Source:
Type:
Vimentin, a major constituent of the intermediate filament family of proteins, is ubiquitously expressed in normal mesenchymal cells and is known to maintain cellular integrity and provide resistance against stress. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure.

In many epithelial-derived tumors (carcinomas), elevated Vimentin expression is often observed in cancer cells that have undergone EMT. This upregulation is characteristic of a shift toward a mesenchymal state, which is associated with reduced cell–cell adhesion and increased motility. Vimentin expression is also noted in the tumor stroma, reflecting the presence and activation of mesenchymal cells such as cancer-associated fibroblasts (CAFs). This dual expression can contribute to the remodeling of the tumor microenvironment.
The degree of Vimentin expression may vary depending on the tumor type, grade, and stage. More aggressive and advanced tumors tend to show higher levels of Vimentin expression.

High Vimentin expression has been correlated with poor clinical outcomes in several cancers, including breast, colorectal, prostate, and lung cancers.
Elevated Vimentin levels are typically associated with higher tumor grade, increased invasiveness, enhanced metastatic potential, and a greater risk of recurrence.
As a component of the EMT signature, high Vimentin expression can serve as an indicator of a more aggressive tumor phenotype and is often associated with reduced overall survival.
- vimentin up-regulation is often used as a marker of EMT in cancer



Scientific Papers found: Click to Expand⟱
1107- CHr,    Chrysin inhibits metastatic potential of human triple-negative breast cancer cells by modulating matrix metalloproteinase-10, epithelial to mesenchymal transition, and PI3K/Akt signaling pathway
- in-vitro, BC, NA
TumCP↓, Apoptosis↑, MMP-10↓, E-cadherin↑, Vim↓, Snail↓, Slug↓, EMT↓,
2785- CHr,    Emerging cellular and molecular mechanisms underlying anticancer indications of chrysin
- Review, Var, NA
*NF-kB↓, *COX2↓, *iNOS↓, angioG↓, TOP1↓, HDAC↓, TNF-α↓, IL1β↓, cardioP↑, RenoP↑, neuroP↑, LDL↓, BioAv↑, eff↑, cycD1/CCND1↓, hTERT/TERT↓, MMP-10↓, Akt↓, STAT3↓, VEGF↓, EGFR↓, Snail↓, Slug↓, Vim↓, E-cadherin↑, eff↑, TET1↑, ROS↑, mTOR↓, PPARα↓, ER Stress↑, Ca+2↑, ERK↓, MMP↑, Cyt‑c↑, Casp3↑, HK2↓, NRF2↓, HO-1↓, MMP2↓, MMP9↓, Fibronectin↓, GRP78/BiP↑, XBP-1↓, p‑eIF2α↑, *AST↓, ALAT↓, ALP↓, LDH↓, COX2↑, Bcl-xL↓, IL6↓, PGE2↓, iNOS↓, DNAdam↑, UPR↑, Hif1a↓, EMT↓, Twist↓, lipid-P↑, CLDN1↓, PDK1↓, IL10↓, TLR4↓, NOTCH1↑, PARP↑, Mcl-1↓, XIAP↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↓, 1,   lipid-P↑, 1,   NRF2↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

MMP↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   HK2↓, 1,   LDH↓, 1,   LDL↓, 1,   PDK1↓, 1,   PPARα↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 1,   Bcl-xL↓, 1,   Casp3↑, 1,   Cyt‑c↑, 1,   hTERT/TERT↓, 1,   iNOS↓, 1,   Mcl-1↓, 1,  

Protein Folding & ER Stress ⓘ

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

DNA Damage & Repair ⓘ

DNAdam↑, 1,   PARP↑, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

EMT↓, 2,   ERK↓, 1,   HDAC↓, 1,   mTOR↓, 1,   NOTCH1↑, 1,   STAT3↓, 1,   TOP1↓, 1,  

Migration ⓘ

Ca+2↑, 1,   CLDN1↓, 1,   E-cadherin↑, 2,   Fibronectin↓, 1,   MMP-10↓, 2,   MMP2↓, 1,   MMP9↓, 1,   Slug↓, 2,   Snail↓, 2,   TET1↑, 1,   TumCP↓, 1,   Twist↓, 1,   Vim↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   EGFR↓, 1,   Hif1a↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↑, 1,   IL10↓, 1,   IL1β↓, 1,   IL6↓, 1,   PGE2↓, 1,   TLR4↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   eff↑, 2,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   ALP↓, 1,   EGFR↓, 1,   hTERT/TERT↓, 1,   IL6↓, 1,   LDH↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   neuroP↑, 1,   RenoP↑, 1,  
Total Targets: 70

Pathway results for Effect on Normal Cells:


Cell Death ⓘ

iNOS↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,  

Clinical Biomarkers ⓘ

AST↓, 1,  
Total Targets: 4

Scientific Paper Hit Count for: Vim, Vimentin
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#:336  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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