6533b857fe1ef96bd12b5179
RESEARCH PRODUCT
INHIBITION OF CELLULAR GROWTH AND STEROID 11β-HYDROXYLATION INRAS-TRANSFORMED ADRENOCORTICAL CELLS BY THE FUNGAL TOXINS BETICOLINS
Jean-pierre BleinClaude HumbertGuo-qing DingB.f. MaumeMarie-louise MilatGabrielle Maumesubject
medicine.medical_treatmentAdrenal Gland NeoplasmsBiologyTransfectionHeterocyclic Compounds 4 or More RingsSteroidlaw.inventionHydroxylationMiceStructure-Activity Relationshipchemistry.chemical_compoundConfocal microscopylawOrganelleTumor Cells CulturedmedicineAnimalsCells CulturedHydroxysteroidsMicroscopy ConfocalDose-Response Relationship DrugCell growthCell BiologyGeneral MedicineMycotoxinsGrowth InhibitorsNeoplasm ProteinsRatsCell Transformation NeoplasticGenes rasAnimals NewbornchemistryBiochemistryCytoplasmAdrenal CortexSteroid 11-beta-HydroxylaseSignal transductionGrowth inhibitionCell Divisiondescription
Abstract The proliferation of GM16 and 4CDTras-transformed newborn rat adrenocortical (RTAC) cells and Y1 mouse adrenal tumor cells was inhibited by beticolins, the fungal toxins extracted fromCercospora beticola, at submicromolar concentrations in a dose-dependent manner. Inhibitory concentrations for half the maximum inhibition were 150, 75 and 25 n M for beticolin-1 and 230, 150 and 50 n M for beticolin-2 in GM16, 4CDT and Y1 cells respectively. Beticolins strongly inhibited the production of 11β-hydroxysteroids on the second and third days of treatment in a dose-dependent manner between 0.1 and 1 μ M . Beticolins were shown by confocal microscopy to be localized in cytoplasmic organelles about 30–40 min after treatment. This finding favors a direct action of beticolins on mitochondrial steroid 11β-hydroxylase albeit another less direct mechanism involving a cytoplasmic signaling pathway cannot be excluded.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 1996-08-01 | Cell Biology International |