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

Miriam Gaggianesi, Federica Chianale, Elena Rainero, Francesca Riboni, Beatrice Perego, Ilaria Gregnanin, Miriam Gaggianesi, Sara Sampietro, Michele Ferrara, Nicoletta Filigheddu, Paolo E. Porporato, Gianluca Baldanzi, Andrea Graziani, Nicola Surico

Risultato della ricerca: Articlepeer review

24 Citazioni (Scopus)

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.
Lingua originaleEnglish
pagine (da-a)1988-1996
Numero di pagine9
RivistaCellular Signalling
Volume23
Stato di pubblicazionePublished - 2011

All Science Journal Classification (ASJC) codes

  • Cell Biology

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