id:"swepub:oai:gup.ub.gu.se/106980"
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- Leung, Kin-Chuen (författare)
Regulation of growth hormone signaling by selective estrogen receptor modulators occurs through suppression of protein tyrosine phosphatases.
- Artikel/kapitelEngelska2007
Förlag, utgivningsår, omfång ...
- The Endocrine Society,2007
Nummerbeteckningar
- LIBRIS-ID:oai:gup.ub.gu.se/106980
- https://gup.ub.gu.se/publication/106980URI
- https://doi.org/10.1210/en.2006-1305DOI
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- Språk:engelska
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- SwePubSwePub
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Anmärkningar
- Activation of the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 5 (STAT5) pathway by GH is terminated by the suppressors of cytokine signaling (SOCSs) and protein tyrosine phosphatases, Src homology 2 domain-containing protein tyrosine phosphatase (SHP)-1 and SHP-2. Based on our recent report that estrogen inhibits GH signaling by stimulating SOCS-2 expression, we investigated the effects of selective estrogen receptor modulators (SERMs) on GH signaling in human embryonic kidney (HEK293) and breast cancer (MDA-MB-231) cells expressing human GH receptor and estrogen receptor-alpha. 17beta-estradiol (E(2)) suppressed GH activation of a STAT5-responsive luciferase reporter and JAK2 phosphorylation in both cell models. 4-hydroxytamoxifen and raloxifene augmented these actions of GH in HEK293 cells but not breast cancer cells. SOCS-2 expression in both cell types was stimulated by E(2) but unaffected by SERMs. In HEK293 cells, SHP-1 was inhibited by raloxifene and 4-hydroxytamoxifen, whereas the latter additionally inhibited SHP-2. The phosphatases were unaffected by E(2). In breast cancer cells, phosphatase activity was not altered by SERMs or E(2). In summary, estrogen inhibited the JAK2/STAT5 signaling of GH and stimulated SOCS-2 expression in both HEK293 and breast cancer cells. By contrast, SERMs augmented GH signaling by reducing SHP activities in HEK293 cells and had no effect on both in breast cancer cells. We provide the first evidence for a novel mechanism regulating GH signaling, in which SERMs enhance GH activation of the JAK2/STAT5 pathway in a cell-type-dependent manner by attenuating protein tyrosine phosphatase activities.
Ämnesord och genrebeteckningar
- MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin Endokrinologi och diabetes hsv//swe
- MEDICAL AND HEALTH SCIENCES Clinical Medicine Endocrinology and Diabetes hsv//eng
- Breast Neoplasms
- Cell Line
- Tumor
- Dactinomycin
- pharmacology
- Estrogen Antagonists
- pharmacology
- Estrogens
- pharmacology
- Human Growth Hormone
- metabolism
- Humans
- Intracellular Signaling Peptides and Proteins
- metabolism
- Janus Kinase 2
- metabolism
- Kidney
- cytology
- Protein Synthesis Inhibitors
- pharmacology
- Protein Tyrosine Phosphatase
- Non-Receptor Type 11
- Protein Tyrosine Phosphatase
- Non-Receptor Type 6
- metabolism
- Protein Tyrosine Phosphatases
- metabolism
- Raloxifene
- pharmacology
- Receptors
- Estrogen
- antagonists & inhibitors
- metabolism
- STAT5 Transcription Factor
- metabolism
- Signal Transduction
- drug effects
- physiology
- Suppressor of Cytokine Signaling Proteins
- metabolism
- Tamoxifen
- pharmacology
Biuppslag (personer, institutioner, konferenser, titlar ...)
- Brce, Jesena (författare)
- Doyle, Nathan (författare)
- Lee, Heather J (författare)
- Leong, Gary M (författare)
- Sjögren, Klara,1970Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för invärtesmedicin,Institute of Medicine, Department of Internal Medicine(Swepub:gu)xsjokl (författare)
- Ho, Ken K Y (författare)
- Göteborgs universitetInstitutionen för medicin, avdelningen för invärtesmedicin (creator_code:org_t)
Sammanhörande titlar
- Ingår i:Endocrinology: The Endocrine Society148:5, s. 2417-230013-72271945-7170
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