Receptor and centriole pathways of steroid action in normal and neoplastic cells.
An experimental system designed for tracing the estradiol kinetics in target cells by specific antibodies has been applied to human breast cancer. Several major defects of the estradiol receptor mechanism have been demonstrated. The detected changes (lack of cytoplasmic receptors, impaired nuclear transfer of estradiol:receptor complexes, and abnormal nuclear retention of these complexes) have been demonstrated in most human breast cancers that appear to be composed of hormone-dependent and autonomous mixed-cell populations. These abnormalities could be the biological background for the overall or partial unresponsiveness of breast cancer to endocrine management. The participation of steroids in the regulation of centriole activities is taken into account since immunoreactive steroids are traceable by UV and electron microscopy at the level of this cell organelle by steroid antibodies. Moreover, the presence of steroids in the pericentriolar material correlates well with the modulating appearance and activity of the centriole throughout the cell cycle. A new centriole pathway is suggested by which steroid hormones can regulate cell proliferation.
D001943:Breast Neoplasms / Q000378:metabolism*; D002455:Cell Division / Q000187:drug effects; D002467:Cell Nucleus / Q000378:metabolism; D002502:Centrioles / Q000187:drug effects / Q000378:metabolism*; D003593:Cytoplasm / Q000378:metabolism; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D009376:Neoplasms, Hormone-Dependent / Q000378:metabolism*; D009940:Organoids / Q000378:metabolism*; D011960:Receptors, Estrogen / Q000378:metabolism*; D013256:Steroids / Q000494:pharmacology*
D011960:Receptors, Estrogen; D013256:Steroids