Flexible Estrogen Receptor Modulators:  Design, Synthesis, and Antagonistic Effects in Human MCF-7 Breast Cancer Cells

2001 ◽  
Vol 44 (7) ◽  
pp. 1072-1084 ◽  
Author(s):  
Mary J. Meegan ◽  
Rosario B. Hughes ◽  
David G. Lloyd ◽  
D. Clive Williams ◽  
Daniela M. Zisterer
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Design Synthesis ◽  
Antagonistic Effects ◽  
Estrogen Receptor Modulators ◽  
Receptor Modulators ◽  
Mcf 7

ChemInform Abstract: Flexible Estrogen Receptor Modulators: Design, Synthesis, and Antagonistic Effects in Human MCF-7 Breast Cancer Cells.

ChemInform ◽  
2010 ◽  
Vol 32 (27) ◽  
pp. no-no
Author(s):  
Mary J. Meegan ◽  
Rosario B. Hughes ◽  
David G. Lloyd ◽  
D. Clive Williams ◽  
Daniela M. Zisterer
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Design Synthesis ◽  
Antagonistic Effects ◽  
Estrogen Receptor Modulators ◽  
Receptor Modulators ◽  
Mcf 7

scholarly journals Regulation of Growth Hormone Signaling by Selective Estrogen Receptor Modulators Occurs through Suppression of Protein Tyrosine Phosphatases

Endocrinology ◽  
2007 ◽  
Vol 148 (5) ◽  
pp. 2417-2423 ◽  
Author(s):  
Kin-Chuen Leung ◽  
Jesena Brce ◽  
Nathan Doyle ◽  
Heather J. Lee ◽  
Gary M. Leong ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tyrosine Phosphatase ◽  
Protein Tyrosine Phosphatases ◽  
Hek293 Cells ◽  
Protein Tyrosine ◽  
Estrogen Receptor Modulators ◽  
Receptor Modulators

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-α. 17β-Estradiol (E2) 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 E2 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 E2. In breast cancer cells, phosphatase activity was not altered by SERMs or E2. 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.

MiRNA-27a sensitizes breast cancer cells to treatment with Selective Estrogen Receptor Modulators

The Breast ◽  
2019 ◽  
Vol 43 ◽  
pp. 31-38 ◽  
Author(s):  
Bojan Ljepoja ◽  
Jonathan García-Roman ◽  
Ann-Katrin Sommer ◽  
Ernst Wagner ◽  
Andreas Roidl
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Selective Estrogen Receptor Modulators ◽  
Estrogen Receptor Modulators ◽  
Receptor Modulators
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