xanthohumol / COX2 Cancer Research Results

Xan, xanthohumol: Click to Expand ⟱

Features:

Xanthohumol is a prenylated chalcone flavonoid derived from hops (Humulus lupulus).

Commonly described actions include:
-Inflammation suppression: attenuation of NF-κB / STAT3 signaling
-Cell-cycle and survival effects: pro-apoptotic signaling, mitochondrial stress
-Angiogenesis inhibition: reduced VEGF signaling in models
-Metabolic stress modulation: interference with lipid and glucose handling
-Redox effects: antioxidant at low/physiologic exposure; pro-oxidant stress at higher concentrations

Importantly, dose, timing, and cellular context determine which mechanism dominates.

Xanthohumol is best described as chemopreventive or chemo-sensitizing, not chemoprotective:

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.

Scientific Papers found: Click to Expand⟱

5015-

Xan,

PEITC,

Comparison of the Impact of Xanthohumol and Phenethyl Isothiocyanate and Their Combination on Nrf2 and NF-κB Pathways in HepG2 Cells In Vitro and Tumor Burden In Vivo

in-vitro,

HCC,

HepG2

NRF2↓, ROS↑, NF-kB↓, COX2↓, Apoptosis↑, NRF2↑, SOD↑, NQO1↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

NQO1↑, 1, NRF2↓, 1, NRF2↑, 1, ROS↑, 1, SOD↑, 1,

Cell Death ⓘ

Apoptosis↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, NF-kB↓, 1,
Total Targets: 8

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