| Features: |
| Zerumbone is a sesquiterpene α,β-unsaturated carbonyl compound derived primarily from Zingiber zerumbet (shampoo ginger). It is one of the most intensively studied dietary terpenoids for anticancer activity, with a strong and internally consistent mechanism-of-action profile across multiple cancer types.
Zerumbone induces intrinsic (mitochondrial) apoptosis via: -↑ ROS generation in cancer cells -Loss of mitochondrial membrane potential -↑ Bax / ↓ Bcl-2 and Bcl-xL -Cytochrome c release -Caspase-9 → caspase-3 activation Zerumbone is a potent NF-κB inhibitor Anti-angiogenic and anti-metastatic effects -Observed actions include: -↓ VEGF and HIF-1α -↓ MMP-2 / MMP-9 -Suppression of EMT markers (N-cadherin, vimentin) -Reduced migration and invasion Zerumbone is a redox-bifunctional agent: In cancer cells: -↑ ROS beyond survival threshold -Triggers mitochondrial collapse In normal cells: -Activates Nrf2 -Induces phase II detox enzymes (HO-1, NQO1, GST) This differential redox response explains selective toxicity. Bioavailability is limited |
| 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. |
| - | in-vitro, | Nor, | RAW264.7 |
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#:384 Target#:66 State#:% Dir#:%
wNotes=0 sortOrder:rid,rpid