Vitexin / COX2/PTGS2 Cancer Research Results

VT, Vitexin: Click to Expand ⟱
Features:

Vitexin - Apigenin-8-C-Glucoside

Alternative Names: Apigenin-8-C-glucoside, apigenin-8-C-β-D-glucopyranoside

Type: Flavone C-glycoside / apigenin derivative

Function: Vitexin is a naturally occurring C-glycosylated flavone in which glucose is attached to apigenin at the C-8 position. It exhibits antioxidant, anti-inflammatory, metabolic, cardiovascular, neuroprotective, and antiproliferative activities and can modulate pathways involving NF-κB, Nrf2/HO-1, MAPK, PI3K/AKT, AMPK, HIF-1α, apoptosis, and oxidative stress.

-see also IsoVitexin

Cancer: Preclinical studies indicate antiproliferative, pro-apoptotic, anti-migratory, anti-invasive, and anti-inflammatory effects across multiple cancer models. Reported mechanisms include modulation of PI3K/AKT, MAPK, NF-κB, HIF-1α, ROS, apoptosis, and cell-cycle signaling. Clinical anticancer efficacy has not been established.

Alzheimer's Disease: Preclinical evidence suggests neuroprotective activity through antioxidant and anti-inflammatory effects, reduction of neuronal injury, regulation of oxidative stress and mitochondrial function, and modulation of signaling pathways relevant to cognitive impairment and amyloid-associated neurotoxicity. Clinical efficacy for Alzheimer's disease has not been established.



COX2/PTGS2, cycloocygenase-2 (Cox-2) mRNA and Cox-2 protein: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Cyclooxygenase-2 (COX-2) is an enzyme that plays a critical role in the conversion of arachidonic acid to prostaglandins, which are lipid compounds involved in various physiological processes, including inflammation, pain, and fever. COX-2 is an inducible enzyme, meaning its expression is typically low in normal tissues but can be upregulated in response to inflammatory stimuli, growth factors, and certain oncogenic signals.
-Cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostaglandin biosynthesis, plays a key role in inflammation and circulatory homeostasis.
-COX-2 is an inducible enzyme that is upregulated in response to pro-inflammatory signals, including cytokines (e.g., IL-1β, TNF-α) and growth factors.

COX-2 is often overexpressed in various tumors, including colorectal, breast, lung, and prostate cancers.
The prostaglandins produced by COX-2, particularly prostaglandin E2 (PGE2), have several effects that can facilitate cancer progression:
Cell Proliferation: PGE2 can promote the proliferation of cancer cells by activating signaling pathways such as the PI3K/Akt and MAPK pathways.
Nonselective NSAIDs, such as aspirin and ibuprofen, inhibit both COX-1 and COX-2. Epidemiological studies have suggested that regular use of NSAIDs may reduce the risk of certain cancers, particularly colorectal cancer.
Drugs specifically targeting COX-2, such as celecoxib, have been developed.

COX-2 and xanthine oxidase are ROS-producing pro-oxidant enzymes that contribute to inflammation. Elevated COX‑2 levels, often found in inflammatory conditions or certain types of cancers, can contribute to increased production of ROS.


Scientific Papers found: Click to Expand⟱
7896- IVT,  VT,    Molecular targets of vitexin and isovitexin in cancer therapy: a critical review
- Review, Var, NA
chemoPv↑, Dose↝, ACE/ACE1↓, Ca+2↓, *iNOS↓, *COX2/PTGS2↓, *ROS↓, *Stroke↓, Apoptosis↑, MMP↓, Bcl-2↓, Casp3↑, Casp9↑, TumAuto↑, HSP90↑, ER Stress↑, Hif1a↓, TumMeta↓, angioG↓, Tf↓, MAPK↓, PI3K↓, Akt↓, β-catenin/ZEB1↓, TumCCA↑, FOXO3↓, mTOR↓,
7902- VT,    Vitexin Protects Against Scopolamine-Induced Cognitive Impairment by Preserving Synaptic Integrity and Modulating Nrf2/HO-1 and NF-κB Signaling Pathways
- in-vivo, AD, NA
*Dose↝, *Learn↑, *memory↑, *AChE↓, *lipid-P↓, *TOS↓, *MDA↓, *ONOO↓, *NO↓, *NOS2↓, *TAC↑, *BDNF↑, *GDNF↑, *PSD95↑, *GFAP↓, *NF-kB↓, *COX2/PTGS2↓, *NRF2↑, *HO-1↑, *neuroP↑, *NeuroI↓,

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:


NA, unassigned(tgid=0)

ACE/ACE1↓, 1,  

Metal & Cofactor Biology(tgid=2)

Tf↓, 1,  

Mitochondria & Bioenergetics(tgid=3)

MMP↓, 1,  

Cell Death(tgid=5)

Akt↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   MAPK↓, 1,  

Protein Folding & ER Stress(tgid=8)

ER Stress↑, 1,   HSP90↑, 1,  

Autophagy & Lysosomes(tgid=9)

TumAuto↑, 1,  

Cell Cycle & Senescence(tgid=11)

TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12)

FOXO3↓, 1,   mTOR↓, 1,   PI3K↓, 1,  

Migration(tgid=13)

Ca+2↓, 1,   TumMeta↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14)

angioG↓, 1,   Hif1a↓, 1,  

Drug Metabolism & Resistance(tgid=21)

Dose↝, 1,  

Functional Outcomes(tgid=23)

chemoPv↑, 1,  
Total Targets: 23

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0)

GDNF↑, 1,   GFAP↓, 1,   Learn↑, 1,   NeuroI↓, 1,   ONOO↓, 1,   Stroke↓, 1,  

Redox & Oxidative Stress(tgid=1)

HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   TAC↑, 1,   TOS↓, 1,  

Cell Death(tgid=5)

iNOS↓, 1,  

Angiogenesis & Vasculature(tgid=14)

NO↓, 1,  

Immune & Inflammatory Signaling(tgid=16)

COX2/PTGS2↓, 2,   NF-kB↓, 1,  

Synaptic & Neurotransmission(tgid=18)

AChE↓, 1,   BDNF↑, 1,   PSD95↑, 1,  

Drug Metabolism & Resistance(tgid=21)

Dose↝, 1,  

Clinical Biomarkers(tgid=22)

NOS2↓, 1,  

Functional Outcomes(tgid=23)

memory↑, 1,   neuroP↑, 1,  
Total Targets: 24

Scientific Paper Hit Count for: COX2/PTGS2, cycloocygenase-2 (Cox-2) mRNA and Cox-2 protein
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#:462  Target#:66  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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