Efp as a primary estrogen‐responsive gene in human breast cancer.

2020 ◽  
Author(s):  
Lungwani Muungo
Keyword(s):  
Breast Cancer ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Promoter Activity ◽  
Breast Tumors ◽  
Human Breast ◽  
Estrogen Responsive Element ◽  
Estrogen Responsive Gene ◽  
Responsive Gene ◽  
Responsive Element

We have previously isolated the efp (estrogenresponsivefinger protein) that is required for the normalestrogen-induced cell proliferation. Here, we show the genomicorganization of the human efp gene which consists of nine exons.The efp mRNA was expressed in human breast tumors and theestrogen-induced expression of the efp was found in MCF-7human breast cancer cells. Moreover, efp promoter activity wasenhanced through the estrogen-responsive element dependent onestrogen and estrogen receptor. These results suggest that the efpcan mediate estrogen actions such as cell growth in human breastcancer as a primary responsive gene.

WISP-2 as a Novel Estrogen-Responsive Gene in Human Breast Cancer Cells

2000 ◽  
Vol 275 (1) ◽  
pp. 108-114 ◽  
Author(s):  
Hidekuni Inadera ◽  
Shin-ichi Hashimoto ◽  
Hong-Yan Dong ◽  
Takuji Suzuki ◽  
Shigenori Nagai ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Estrogen Responsive Gene ◽  
Responsive Gene

scholarly journals MEK inhibition leads to lysosome-mediated Na+/I− symporter protein degradation in human breast cancer cells

2013 ◽  
Vol 20 (2) ◽  
pp. 241-250 ◽  
Author(s):  
Zhaoxia Zhang ◽  
Sasha Beyer ◽  
Sissy M Jhiang
Keyword(s):  
Breast Cancer ◽  
Cell Surface ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Breast Tumors ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Iodide Uptake ◽  
Mek Inhibition ◽  
Protein Levels

The Na+/I−symporter (NIS (SLC5A5)) is a transmembrane glycoprotein that mediates active iodide uptake into thyroid follicular cells. NIS-mediated iodide uptake in thyroid cells is the basis for targeted radionuclide imaging and treatment of differentiated thyroid carcinomas and their metastases. Furthermore, NIS is expressed in many human breast tumors but not in normal non-lactating breast tissue, suggesting that NIS-mediated radionuclide uptake may also allow the imaging and targeted therapy of breast cancer. However, functional cell surface NIS expression is often low in breast cancer, making it important to uncover signaling pathways that modulate NIS expression at multiple levels, from gene transcription to posttranslational processing and cell surface trafficking. In this study, we investigated NIS regulation in breast cancer by MAPK/extracellular signal-regulated kinase (ERK) kinase (MEK) signaling, an important cell signaling pathway involved in oncogenic transformation. We found that MEK inhibition decreased NIS protein levels in all-trans retinoic acid/hydrocortisone-treated MCF-7 cells as well as human breast cancer cells expressing exogenous NIS. The decrease in NIS protein levels by MEK inhibition was not accompanied by a decrease inNISmRNA or a decrease inNISmRNA export from the nucleus to the cytoplasm. NIS protein degradation upon MEK inhibition was prevented by lysosome inhibitors but not by proteasome inhibitors. Interestingly, NIS protein level was correlated with MEK/ERK activation in human breast tumors from a tissue microarray. Taken together, MEK activation appears to play an important role in maintaining NIS protein stability in human breast cancers.

The role of atypical chemokine receptor-1 in breast cancer immune response.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e23072-e23072 ◽  
Author(s):  
Rachel Martini ◽  
Petros Nikolinakos ◽  
Jamie Hodgson ◽  
Brittany Jenkins ◽  
Melissa Davis
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Chemokine Receptor ◽  
Immune Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Breast Tumors ◽  
Human Breast ◽  
Inflammatory Chemokines

e23072 Background: Interactions between chemokines and their receptors can regulate anti-tumor response by influencing the migration of immune cells. Atypical Chemokine Receptor 1 (ACKR1/DARC), a genetically diverse transmembrane GPCR, acts as a decoy receptor for a variety of CXC and CC chemokines, including those with pro-malignant and pro-inflammatory effects, such as CCL2 and CXCL8 . The purpose of this study is to determine if the migration of tumor-associated immune cells is unique based on epithelial ACKR1 expression on breast cancer cells, and if this association is correlated to an increase in pro-malignant chemokines, survival, or race. Methods: Immunohistochemistry techniques were used to determine expression of ACKR1 on primary breast tumors, along with T-cells, B-cells, dendritic cells, and macrophages. Concentrations of pro-inflammatory chemokines in circulation were determined using a Luminex-based immunoassay. In silco analyses were performed to determine associations between ACKR1 tumor status, race, and survival. Finally, using human breast cancer cell lines and immunofluorescence techniques, co-localization between ACKR1 and pro-inflammatory chemokines was investigated. Results: Results from these tests indicate that there is differential infiltration of immune cell types in tumors expressing ACKR1, , which were not detected in ACKR1 negative tumors. Significantly increased circulating CCL2 and CXCL8 chemokine levels we also determined to be positively correlated with ACKR1 expression in primary breast tumors. Survival analyses showed a significantly increased relapse free survival in patients having tumors with high ACKR1 expression, while investigations into racial differences revealed a significant race effect, with Caucasians having higher ACKR1 levels on their tumors than African-Americans. Finally, co-localization between ACKR1 with CCL2 and CXCL8 is observed in cultured human breast cancer cells. Conclusions: tumors positively expressing ACKR1 to have a more favorable prognosis suggest that a role of ACKR1 on breast tumor cells is to sequester pro-inflammatory chemokines in the tumor microenvironment, recruiting a distinct subset of tumor-associated immune cells.

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