Diacylglycerol kinase α mediatses 17-β-estradiol-induced proliferation, motility, and anchorage-independent growth of Hec-1A endometrial cancer cell line through the G protein-coupled estrogen receptor GPR30

التفاصيل البيبلوغرافية
العنوان: Diacylglycerol kinase α mediatses 17-β-estradiol-induced proliferation, motility, and anchorage-independent growth of Hec-1A endometrial cancer cell line through the G protein-coupled estrogen receptor GPR30
المؤلفون: Michele Ferrara, Nicola Surico, Andrea Graziani, Ilaria Gregnanin, Gianluca Baldanzi, Sara Sampietro, Paolo E. Porporato, Nicoletta Filigheddu, Beatrice Perego, Miriam Gaggianesi, Francesca Riboni, Federica Chianale, Elena Rainero
المساهمون: Filigheddu N., Sampietro S., Chianale F., Porporato P.E., Gaggianesi M., Gregnanin I., Rainero E., Ferrara M., Perego B., Riboni F., Baldanzi G., Graziani A., Surico N., Filigheddu, Nicoletta, Sampietro, Sara, Chianale, Federica, Porporato, Paolo E., Gaggianesi, Miriam, Gregnanin, Ilaria, Rainero, Elena, Ferrara, Michele, Perego, Beatrice, Riboni, Francesca, Baldanzi, Gianluca, Graziani, Andrea, Surico, Nicola
بيانات النشر: ELSEVIER SCIENCE INC, 2011.
سنة النشر: 2011
مصطلحات موضوعية: medicine.medical_specialty, GPR30, medicine.drug_class, Cell Survival, Diacylglycerol kinase, Motility, Estrogen receptor, Enzyme Assay, Endometrial carcinoma, Biology, Quinazolinone, Receptors, G-Protein-Coupled, Piperidine, Piperidines, Cell Movement, Internal medicine, Cell Line, Tumor, medicine, Cell Adhesion, Humans, Endometrial Neoplasm, Enzyme Assays, Quinazolinones, Cell Proliferation, Estradiol, Cell growth, Kinase, Cell Biology, Estrogen, Endometrial Neoplasms, Cell biology, Enzyme Activation, Lipoprotein Lipase, Endocrinology, Receptors, Estrogen, Gene Knockdown Techniques, Gene Knockdown Technique, Female, RNA Interference, Signal transduction, GPER, Human
الوصف: Increased levels of endogenous and/or exogenous estrogens are one of the well known risk factors of endometrial cancer. Diacylglycerol kinases (DGKs) are a family of enzymes which phosphorylate diacylglycerol (DAG) to produce phosphatidic acid (PA), thus turning off and on DAG-mediated and PA-mediated signaling pathways, respectively. DGK α activity is stimulated by growth factors and oncogenes and is required for chemotactic, proliferative, and angiogenic signaling in vitro. Herein, using either specific siRNAs or the pharmacological inhibitor R59949, we demonstrate that DGK α activity is required for 17-β-estradiol (E2)-induced proliferation, motility, and anchorage-independent growth of Hec-1A endometrial cancer cell line. Impairment of DGK α activity also influences basal cell proliferation and growth in soft agar of Hec-1A, while it has no effects on basal cell motility. Moreover, we show that DGK α activity induced by E2, as well as its observed effects, are mediated by the G protein-coupled estrogen receptor GPR30 (GPER). These findings suggest that DGK α may be a potential target in endometrial cancer therapy. © 2011 Elsevier Inc.
اللغة: English
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::845ef4f43932561599b4e835fac30682Test
http://hdl.handle.net/10447/404410Test
حقوق: OPEN
رقم الانضمام: edsair.doi.dedup.....845ef4f43932561599b4e835fac30682
قاعدة البيانات: OpenAIRE