Use of cDNA cloning to study the mechanism of action of glucocorticoid hormones at the molecular level.
We have previously described a dramatic phenomenon of phenotypic reversion (tumor to normal) caused by glucocorticoid hormones in C6/ST1 rat glioma cells, but not in their hormone-resistant C6/P7 counterpart. Blind cDNA cloning was adopted to search for glucocorticoid-regulated gene sequences responsible for this phenotype reversion. Differential hybridization and differential display of RNA were used in parallel to isolate a number of cDNA clones that were characterized by DNA sequencing and Northern blot analysis. This approach was coupled to the analysis of known growth control genes (oncogenes, tumor suppressor genes, cyclins, cyclin-dependent kinases, other kinases). Glucocorticoid target genes isolated from this cell system are likely to be good anti-tumor candidate molecules which can be used in tumor therapy and anti-tumor drug design.
Armelin
M C
MC
Instituto de Química, Universidade de São Paulo, Brasil. mcsarmel@quim.iq.usp.br
Sasahara
R M
RM
Flatschart
R
R
Vedoy
C
C
D000818:Animals; D002453:Cell Cycle / Q000235:genetics*; D002455:Cell Division; D002471:Cell Transformation, Neoplastic / Q000235:genetics*; D003001:Cloning, Molecular; D018076:DNA, Complementary; D015972:Gene Expression Regulation, Neoplastic / Q000235:genetics*; D018390:Gene Targeting; D005938:Glucocorticoids / Q000235:genetics* / Q000502:physiology; D009369:Neoplasms / Q000235:genetics / Q000473:pathology; D051381:Rats
D018076:DNA, Complementary; D005938:Glucocorticoids