title: Overlapping nongenomic and genomic actions of thyroid hormone and steroids.
abstract: Nuclear receptors for thyroid hormone and steroids are members of a receptor superfamily with similar molecular organization, but discrete transcriptional functions that define genomic actions of these nonpeptide hormones. Nongenomic actions of thyroid hormone and estrogens and androgens are initiated outside the nucleus, at receptors in the plasma membrane or in cytoplasm; these actions are largely regarded to be unique to the respective hormones. However, there is an increasing number of descriptions of overlapping nongenomic and genomic effects of thyroid hormone and estrogens and testosterone. These effects are concentrated in tumor cells, where, for example, estrogens and thyroid hormone have similar mitogen-activate protein kinase (MAPK)-dependent proliferative actions on ERα-positive human breast cancer cells, and where dihydrotestosterone also can stimulate proliferation. Steroids and thyroid hormone have similar anti-apoptotic effects in certain tumors. But thyroid hormone and steroids also have overlapping or interacting nongenomic and genomic actions in heart and brain cells. These various effects of thyroid hormone and estrogens and androgens are reviewed here and their possible clinical consequences are enumerated.
authors.affiliation: Signal Transduction Laboratory, Ordway Research Institute, Albany, NY 12208, USA. pdavis@ordwayresearch.org
authors.forename: Paul J
authors.initials: PJ
authors.lastname: Davis
authors.forename: Hung-Yun
authors.initials: HY
authors.lastname: Lin
authors.forename: Shaker A
authors.initials: SA
authors.lastname: Mousa
authors.forename: Mary K
authors.initials: MK
authors.lastname: Luidens
authors.forename: Aleck A
authors.initials: AA
authors.lastname: Hercbergs
authors.forename: Martin
authors.initials: M
authors.lastname: Wehling
authors.forename: Faith B
authors.initials: FB
authors.lastname: Davis
mesh_terms: D000818:Animals; D017209:Apoptosis; D001943:Breast Neoplasms / Q000378:metabolism / Q000473:pathology; D006332:Cardiomegaly / Q000378:metabolism; D049109:Cell Proliferation; D047628:Estrogen Receptor alpha / Q000235:genetics / Q000502:physiology; D004967:Estrogens / Q000235:genetics / Q000502:physiology*; D005260:Female; D006801:Humans; D008297:Male; D009376:Neoplasms, Hormone-Dependent / Q000378:metabolism / Q000473:pathology; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D013739:Testosterone / Q000502:physiology*; D013961:Thyroid Gland / Q000166:cytology / Q000378:metabolism; D013963:Thyroid Hormones / Q000235:genetics / Q000502:physiology*; D014158:Transcription, Genetic; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000502:physiology
chemical_list: D047628:Estrogen Receptor alpha; D004967:Estrogens; D013963:Thyroid Hormones; D016159:Tumor Suppressor Protein p53; D013739:Testosterone; D058570:TOR Serine-Threonine Kinases