COX2 Cancer Research Results

COX2, 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.
GBM, Glioblastoma: Click to Expand ⟱
Glioblastoma is a fast-growing and aggressive brain tumor.
Scientific Papers found: Click to Expand⟱
2127- TQ,    Therapeutic Potential of Thymoquinone in Glioblastoma Treatment: Targeting Major Gliomagenesis Signaling Pathways
- Review, GBM, NA
chemoP↑, ChemoSen↑, BioAv↑, PTEN↑, PI3K↓, Akt↓, TumCCA↓, NF-kB↓, p‑Akt↓, p65↓, XIAP↓, Bcl-2↓, COX2↓, VEGF↓, mTOR↓, RAS↓, Raf↓, MEK↓, ERK↓, MMP2↓, MMP9↓, TumCMig↓, TumCI↓, Casp↑, cl‑PARP↑, ROS⇅, ROS↑, MMP↓, eff↑, Telomerase↓, DNAdam↑, Apoptosis↑, STAT3↓, RadioS↑,
1218- VitC,  ASA,    Ascorbic acid enhances the inhibitory effect of aspirin on neuronal cyclooxygenase-2-mediated prostaglandin E2 production
- in-vitro, GBM, SK-N-SH
PGE2↓, COX2↓,

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 ⓘ

ROS↑, 1,   ROS⇅, 1,  

Mitochondria & Bioenergetics ⓘ

MEK↓, 1,   MMP↓, 1,   Raf↓, 1,   XIAP↓, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Telomerase↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   mTOR↓, 1,   PI3K↓, 1,   PTEN↑, 1,   RAS↓, 1,   STAT3↓, 1,  

Migration ⓘ

MMP2↓, 1,   MMP9↓, 1,   TumCI↓, 1,   TumCMig↓, 1,  

Angiogenesis & Vasculature ⓘ

VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   NF-kB↓, 1,   p65↓, 1,   PGE2↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↑, 1,   eff↑, 1,   RadioS↑, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,  
Total Targets: 35

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: COX2, 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:27  Cells:%  prod#:%  Target#:66  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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