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1. Diacylglycerol kinase α mediates 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.

Author

Filigheddu N, Sampietro S, Chianale F, Porporato PE, Gaggianesi M, Gregnanin I, Rainero E, Ferrara M, Perego B, Riboni F, Baldanzi G, Graziani A, and Surico N

Subjects
Cell Line, Tumor, Cell Survival, Endometrial Neoplasms, Enzyme Activation, Enzyme Assays, Female, Gene Knockdown Techniques, Humans, Lipoprotein Lipase antagonists & inhibitors, Lipoprotein Lipase genetics, Piperidines pharmacology, Quinazolinones pharmacology, RNA Interference, Receptors, Estrogen, Receptors, G-Protein-Coupled genetics, Cell Adhesion, Cell Movement drug effects, Cell Proliferation drug effects, Estradiol pharmacology, Lipoprotein Lipase metabolism, Receptors, G-Protein-Coupled metabolism
Abstract

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., (Copyright © 2011 Elsevier Inc. All rights reserved.)

Published
2011
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2. 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

Author

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, 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, and Surico, Nicola

Subjects
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
Abstract

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.

Published
2011

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