[CAS NO. 71030-37-0] 12-HETE
PRODUCTS SPECIFICATIONS [71030-37-0]
DESCRIPTION [71030-37-0]
Overview
| MDL | - |
|---|---|
| Molecular Weight | 320.47 |
| Molecular Formula | C20H32O3 |
| SMILES | CCCCC/C=C\CC(O)/C=C/C=C\C/C=C\CCCC(O)=O |
Summary
12-HETE, a major metabolic product of arachidonic acid using 12-LOX catalysis, inhibits cell apoptosis in a dose-dependent manner. 12-HETE promotes the activation and nuclear translocation of NF-κB through the integrin-linked kinase (ILK) pathway [1] .12-HETE has both anti-thrombotic and pro-thrombotic effects [2] . 12-HETE is a neuromodulator [3] .
In Vitro
12-HETE participates in the inhibition of cell
apoptosis
by activating the ILK/NF-κB pathway, implying an important underlying mechanism that promotes the survival of ovarian
cancer
cells. 12-HETE facilitates cell survival by activating the integrin-linked kinase/NF-κB pathway in ovarian
cancer
. 12-HETE protects against cell
apoptosis
in ovarian
cancer
cells in a concentration-dependent manner. 12-HETE (1 µM) significantly decreases the activation of
caspase-3
induced by serum deprivation (SD).12-HETE represses the increased activity of
caspase-3
induced by SD in a concentration-dependent manner, with an IC
50
value of 1.13 µM
[1]
.
12-HETE (1 µM) facilitates the activation and nuclear translocation of
NF-κB
via ILK in ovarian
cancer
cells
[1]
.
12-HETE inhibits
insulin
secretion, reduces metabolic activity and induces cell death in human islets. 12-HETE increases bovine platelet aggregation induced by
thrombin
and inhibits prostaglandin E1-induced elevation of intracellular cAMP levels. 12-HETE inhibits washed platelet (WP) aggregation
[2]
.
The neuronal effects of 12-HETE include attenuation of calcium influx and glutamate release as well as inhibition of AMPA receptor (AMPA-R) activation
[3]
.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Cell Viability Assay [1]
| Cell Line: | Ovarian cancer OVCAR-3 and SKOV3 cells |
| Concentration: | 0, 0.2, 0.5, and 1 µM |
| Incubation Time: | 0, 24, 48, 72, and 96 hours |
| Result: |
Inhibited the decrease in cell viability induced by SD in a dose-dependent manner.
1 µM 12-HETE treatment significantly mitigated the decrease in cell viability under conditions of SD. |
Western Blot Analysis [1]
| Cell Line: | Ovarian cancer OVCAR-3 and SKOV3 cells |
| Concentration: | 1 µM |
| Incubation Time: | |
| Result: |
Led to increased levels of NF-κB p65 phosphorylation.
Caused a significant increase in the protein levels of nuclear NF-κB p65, which was accompanied by decreased levels of NF-κB p65 in the cytoplasm. |
Appearance
Liquid
Shipping
Room temperature in continental US; may vary elsewhere.
Storage
Solution, -20°C, 2 years
References
- [1] Qian Liu, et al. 12-HETE facilitates cell survival by activating the integrin-linked kinase/NF-κB pathway in ovarian cancer. Cancer Manag Res. 2018 Nov 16;10:5825-5838.
- [2] Benedetta Porro, et al. Analysis, physiological and clinical significance of 12-HETE: a neglected platelet-derived 12-lipoxygenase product. J Chromatogr B Analyt Technol Biomed Life Sci. 2014 Aug 1;964:26-40.
- [3] Aidan J Hampson, et al. 12-hydroxyeicosatetrenoate (12-HETE) attenuates AMPA receptor-mediated neurotoxicity: evidence for a G-protein-coupled HETE receptor. J Neurosci. 2002 Jan 1;22(1):257-64.