Differential initiation of translation of a single estrogen receptor mRNA could explain some estradiol resistance cases.
Cell response to steroid stimulation is generally acknowledged to be mediated by an intracellular protein known as a receptor. Response intensity is related to the affinity of the receptor and to the number of sites occupied by its specific ligand. Although verified in the majority of experimental and clinical studies, certain phenomena of steroid hormone resistance would seem to challenge this assertion. Application of gene molecular biology to determine the action mechanisms of steroid hormones has partially explained cell resistance in terms of genetic modifications. The work presented here shows that in certain cases, estrogen resistance could be explained by regulation of translation of the single messenger RNA coding for the receptor.
Toulas
C
C
Institut L.-Bugnard, Laboratoire d'Endocrinologie Expérimentale INSERM CJF 9103, CHU Rangueil, Toulouse, France.
Barraillé
P
P
Delassus
F
F
Bayard
F
F
Prats
H
H
Faye
J C
JC
D000818:Animals; D002460:Cell Line; D004351:Drug Resistance; D004700:Endocrine System Diseases / Q000235:genetics*; D004958:Estradiol / Q000494:pharmacology*; D006801:Humans; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000235:genetics*; D011960:Receptors, Estrogen / Q000235:genetics*
D012333:RNA, Messenger; D011960:Receptors, Estrogen; D004958:Estradiol