PMID- 8314862
OWN - NLM
STAT- MEDLINE
DCOM- 19930727
LR  - 20141120
IS  - 0021-9541 (Print)
IS  - 0021-9541 (Linking)
VI  - 156
IP  - 1
DP  - 1993 Jul
TI  - Characterization of selective glucocorticoid-dependent responses in a 
      glucocorticoid-resistant smooth muscle tumor cell line.
PG  - 88-95
AB  - The DDT1 MF2 smooth muscle cell line was derived from an 
      estrogen/androgen-induced leiomyosarcoma arising in the hamster ductus deferens. 
      Growth of this cell line is arrested in G0/G1 by treatment with glucocorticoids. 
      To facilitate the study of the mechanism of glucocorticoid-induced cell growth 
      arrest, a glucocorticoid-resistant variant cell line, DDT1 MF2 GR1 (GR1), was 
      developed by genetic selection. Growth of this mutant cell line is completely 
      resistant to the inhibitory action of glucocorticoids. However, we now 
      demonstrate that both primary and secondary glucocorticoid-induced events still 
      exist in the GR1 cell line. By analyzing the expression and genetic pattern of 
      glucocorticoid receptor, no detectable rearrangement of the glucocorticoid 
      receptor gene was found although the expression of both mRNA and protein levels 
      of the receptor were lower in the variant compared to wild-type cells. In 
      addition, we found that the expression of two growth-associated genes, Ha-ras and 
      transforming growth factor beta 1 (TGF-beta 1) are down-regulated by 
      glucocorticoids in wild-type DDT1 MF2 cells but not in GR1 cells. These results 
      indicated that the function or activity of glucocorticoid receptor in the GR1 
      cells is not qualitatively altered. Our data suggest that a lower glucocorticoid 
      receptor level is not the real cause or at least not the single cause for the GR1 
      cell's loss of sensitivity to the inhibitory action of glucocorticoid. Instead, 
      we postulate the existence of a defect downstream of the primary site of action 
      of glucocorticoid receptor complexes in GR1 cells.
FAU - Fan, W
AU  - Fan W
AD  - Department of Medicine, Medical University of South Carolina, Charleston 29425.
FAU - Cooper, T M
AU  - Cooper TM
FAU - Norris, J S
AU  - Norris JS
LA  - eng
GR  - CA-499949/CA/NCI NIH HHS/United States
GR  - CA-52085/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Glucocorticoids)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
GS  - hGSTYBX
GS  - ras
MH  - Animals
MH  - Cell Division/drug effects
MH  - Cricetinae
MH  - Drug Resistance
MH  - Gene Expression/drug effects
MH  - Genes
MH  - Genes, ras
MH  - Glucocorticoids/*pharmacology
MH  - In Vitro Techniques
MH  - Leiomyosarcoma
MH  - Muscle, Smooth/*cytology
MH  - RNA, Messenger/genetics
MH  - Receptors, Glucocorticoid/genetics/metabolism
MH  - Restriction Mapping
MH  - Transforming Growth Factor beta/genetics
MH  - Tumor Cells, Cultured
EDAT- 1993/07/01 00:00
MHDA- 1993/07/01 00:01
CRDT- 1993/07/01 00:00
PHST- 1993/07/01 00:00 [pubmed]
PHST- 1993/07/01 00:01 [medline]
PHST- 1993/07/01 00:00 [entrez]
AID - 10.1002/jcp.1041560113 [doi]
PST - ppublish
SO  - J Cell Physiol. 1993 Jul;156(1):88-95. doi: 10.1002/jcp.1041560113.