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.
AML, Acute Myeloid Leukemia: Click to Expand ⟱
Acute Myeloid Leukemia
Scientific Papers found: Click to Expand⟱
1089- MAG,    Magnolol potently suppressed lipopolysaccharide-induced iNOS and COX-2 expression via downregulating MAPK and NF-κB signaling pathways
- in-vitro, AML, RAW264.7
p‑IκB↓, NF-kB↓, p‑ERK↓, p‑JNK↓, p‑PI3K↓, p‑Akt↓, iNOS↓, COX2↓,
42- QC,    Quercetin induces apoptosis by activating caspase-3 and regulating Bcl-2 and cyclooxygenase-2 pathways in human HL-60 cells
- in-vitro, AML, HL-60
Bcl-2↓, BAX↑, Casp3↑, COX2↓,
3429- TQ,    Thymoquinone exerts potent growth-suppressive activity on leukemia through DNA hypermethylation reversal in leukemia cells
- in-vitro, AML, NA - in-vivo, NA, NA
DNMT1↓, Sp1/3/4↓, NF-kB↓, Apoptosis↑, Casp↑, Bcl-xL↓, COX2↓, iNOS↓, 5LO↓, TNF-α↓, cycD1/CCND1↓, BioAv↝, TumCG↓,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Cell Death ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp↑, 1,   Casp3↑, 1,   iNOS↓, 2,   p‑JNK↓, 1,  

Kinase & Signal Transduction ⓘ

Sp1/3/4↓, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,  

Cell Cycle & Senescence ⓘ

cycD1/CCND1↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

p‑ERK↓, 1,   p‑PI3K↓, 1,   TumCG↓, 1,  

Migration ⓘ

5LO↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 3,   p‑IκB↓, 1,   NF-kB↓, 2,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↝, 1,  
Total Targets: 21

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
1 Magnolol
1 Quercetin
1 Thymoquinone
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:2  Cells:%  prod#:%  Target#:66  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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