Expression of c-myc gene in human ovary carcinoma cells treated with vanadate
- Engelhardt Inst. of Molecular Biology, Moscow (USSR)
The widely accepted hypothesis of vanadate action on cells postulates that this ion inhibits protein phosphatase(s) that dephosphorylates protein phosphotyrosine residues. This inhibition causes tyrosine hyperphosphorylation of cell proteins followed by changes in physiological action of phosphoproteins resulting in stimulation of cell proliferation, expression of protooncogenes, and transient cell transformation. The authors have found that treatment of human ovary carcinoma (CaOv) cells with vanadate causes the increase in total protein phosphorylation from 1.5- to 2.0-fold whereas the ratio between phosphoserine, phosphothreonine, and phosphotyrosine content remains unchanged. At the same time, enhancement of c-myc gene expression (not c-fos) was observed. Hence, the increase in the ratio of phosphotyrosine to phosphoserine and phosphothreonine is not an obligatory intermediate stage before vanadate-dependent activation of c-myc expression.
- OSTI ID:
- 5312681
- Journal Information:
- Experimental Cell Research; (United States), Vol. 188:1; ISSN 0014-4827
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
ONCOGENES
CHEMICAL ACTIVATION
VANADATES
BIOLOGICAL EFFECTS
CARCINOMAS
CELL PROLIFERATION
GENE REGULATION
OVARIES
SERINE
THREONINE
TYROSINE
WOMEN
AMINO ACIDS
ANIMALS
BODY
CARBOXYLIC ACIDS
DISEASES
FEMALE GENITALS
FEMALES
GENES
GONADS
HYDROXY ACIDS
MAMMALS
MAN
NEOPLASMS
ORGANIC ACIDS
ORGANIC COMPOUNDS
ORGANS
OXYGEN COMPOUNDS
PRIMATES
TRANSITION ELEMENT COMPOUNDS
VANADIUM COMPOUNDS
VERTEBRATES
550200* - Biochemistry