P2-01-19: Expression of Receptor Like Protein Tyrosine Phosphatases mu (PTPRM) in Breast Cancer and the Biological Effects of PTPRM on Breast Cancer Cells.

2011 ◽  
Author(s):  
P-H Sun ◽  
L Ye ◽  
RE Mansel ◽  
WG Jiang
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Biological Effects ◽  
Protein Tyrosine Phosphatases ◽  
Tyrosine Phosphatases ◽  
Protein Tyrosine

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.

scholarly journals Glucocorticoid receptor–IRS-1 axis controls EMT and the metastasis of breast cancers

2019 ◽  
Vol 11 (12) ◽  
pp. 1042-1055 ◽  
Author(s):  
Weiwei Shi ◽  
Dongmei Wang ◽  
Xinwang Yuan ◽  
Yi Liu ◽  
Xiaojie Guo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Glucocorticoid Receptor ◽  
Cell Survival ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Biological Effects ◽  
Ectopic Expression ◽  
Metastatic Breast ◽  
Mesenchymal Transition ◽  
Expression Levels

Abstract Glucocorticoid receptor (GR) is involved in the transcriptional regulation of genes that are important for various biological functions, including tumor growth and metastatic progression. However, the cellular and biological effects of GR remain poorly understood. Here, we investigated the role of GR and its underlying mechanism in mediating breast cancer cell survival and metastasis. We observed that the GR levels were increased in drug-resistant breast cancer cells and in metastatic breast cancer samples. GR promoted tumor cell invasion and lung metastasis in vivo. The GR expression levels were negatively correlated with the survival rates of breast cancer patients. Both ectopic expression and knockdown of GR revealed that GR is a strong inducer of epithelial-to-mesenchymal transition (EMT), which is consistent with its effects on cell survival and metastasis. GR suppressed the expression of insulin receptor substrate 1 (IRS-1) by acting as an IRS-1 transcriptional repressor. In addition, GR has an opposite effect on the expression levels of IRS-2, indicating that GR is able to differentially regulate the IRS-1 and IRS-2 expression. The cellular and biological effects elicited by GR were consistent with the reduced levels of IRS-1 observed in cancer cells, and GR-mediated IRS-1 suppression activated the ERK2 MAP kinase pathway, which is required for GR-mediated EMT. Taken together, our results indicate that GR–IRS-1 signaling axis plays an essential role in regulating the survival, invasion, and metastasis of breast cancer cells.

scholarly journals Cichorins D–F: Three New Compounds from Cichorium intybus and Their Biological Effects

Molecules ◽  
2020 ◽  
Vol 25 (18) ◽  
pp. 4160
Author(s):  
Muhammad Farooq Khan ◽  
Fahd A. Nasr ◽  
Omar M. Noman ◽  
Nouf Abdulaziz Alyhya ◽  
Iftikhar Ali ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Biological Effects ◽  
2D Nmr ◽  
Cichorium Intybus ◽  
Traditional Medicines ◽  
Wide Range ◽  
Sarcoma Cells ◽  
New Compounds

Cichorium intybus L., (chicory) is employed in various traditional medicines to treat a wide range of diseases and disorders. In the current investigation, two new naphthalane derivatives viz., cichorins D (1) and E (2), along with one new anthraquinone cichorin F (3), were isolated from Cichorium intybus. In addition, three previously reported compounds viz., β-sitosterol (4), β-sitosterol β-glucopyranoside (5), and stigmasterol (6) were also isolated from Cichorium intybus. Their structures were established via extensive spectroscopic data, including 1D (1H and 13C) and 2D NMR (COSY, HSQC and HMBC), and ESIMS. Cichorin E (2) has a weak cytotoxic effect on breast cancer cells (MDA-MB-468: IC50: 85.9 µM) and Ewing’s sarcoma cells (SK-N-MC: IC50: 71.1 µM); cichorin F (3) also illustrated weak cytotoxic effects on breast cancer cells (MDA-MB-468: IC50: 41.0 µM and MDA-MB-231: IC50: 45.6 µM), and SK-N-MC cells (IC50: 71.9 µM). Moreover compounds 1–3 did not show any promising anthelmintic effects.

scholarly journals Focal adhesion kinase regulates the phosphorylation protein tyrosine phosphatase-α at Tyr789 in breast cancer cells

2015 ◽  
Vol 11 (6) ◽  
pp. 4303-4308 ◽  
Author(s):  
XU-QIAN FANG ◽  
XIANG-FAN LIU ◽  
LING YAO ◽  
CHANG-QIANG CHEN ◽  
JIA-FEI LIN ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Focal Adhesion Kinase ◽  
Cancer Cells ◽  
Focal Adhesion ◽  
Protein Tyrosine Phosphatase ◽  
Breast Cancer Cells ◽  
Tyrosine Phosphatase ◽  
Protein Tyrosine

scholarly journals Breast Tumor Kinase (Protein Tyrosine Kinase 6) Regulates Heregulin-Induced Activation of ERK5 and p38 MAP Kinases in Breast Cancer Cells

2007 ◽  
Vol 67 (9) ◽  
pp. 4199-4209 ◽  
Author(s):  
Julie Hanson Ostrander ◽  
Andrea R. Daniel ◽  
Kristopher Lofgren ◽  
Celina G. Kleer ◽  
Carol A. Lange
Keyword(s):  
Breast Cancer ◽  
Tyrosine Kinase ◽  
Cancer Cells ◽  
Breast Tumor ◽  
Breast Cancer Cells ◽  
Protein Tyrosine Kinase ◽  
Map Kinases ◽  
Protein Tyrosine ◽  
Breast Tumor Kinase

scholarly journals Role of the Protein Tyrosine Kinase Syk in Regulating Cell-Cell Adhesion and Motility in Breast Cancer Cells

2009 ◽  
Vol 7 (5) ◽  
pp. 634-644 ◽  
Author(s):  
Xiaoying Zhang ◽  
Ulka Shrikhande ◽  
Bethany M. Alicie ◽  
Qing Zhou ◽  
Robert L. Geahlen
Keyword(s):  
Breast Cancer ◽  
Cell Adhesion ◽  
Tyrosine Kinase ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Protein Tyrosine Kinase ◽  
Protein Tyrosine ◽  
Cell Cell
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