F-prostanoid receptor alters adhesion, morphology and migration of endometrial adenocarcinoma cells.

Abstract:

:Cellular adhesion to extracellular matrix is a central phenomenon for the maintenance of tissue integrity and cellular movement. Collectively, these processes are regulated by a fine-tuned balance between the formation and loosening of adhesive contacts, a process involving integrins, and the elevation and diminution of cytoplasmic signalling molecules. We demonstrate that prostaglandin (PG) F(2alpha) stimulation rapidly increases the capacity of Ishikawa cells stably expressing the F-prostanoid receptor (FPS) to adhere to vitronectin. Coincident with this elevation in matrix adhesion, we demonstrate a profound PGF(2alpha)-induced alteration in cytoskeletal remodelling, characterized by polymerization of the actin cytoskeleton and recruitment of focal adhesion kinase at focal adhesions and enhanced cell migration. Moreover, we show that these PGF(2alpha)-induced alterations in adhesion and morphology on vitronectin and migration could be abolished by cultivating FPS cells in the presence of integrin alphavbeta3 antibody or alphavbeta3-directed tetrapeptide arg-gly-asp-ser or inhibition of FP receptor signalling with the FP receptor antagonist, chemical disruptors of the phospholipase C-beta, protein kinase A, c-Src and epidermal growth factor receptor kinase pathways or inhibition of the monomeric G proteins Rho, Rac and CDC42. These results reveal a mechanism by which prostanoids regulate cell movement, which may be relevant to pathologies of the endometrium.

journal_name

Oncogene

journal_title

Oncogene

authors

Sales KJ,Boddy SC,Jabbour HN

doi

10.1038/sj.onc.1210883

subject

Has Abstract

pub_date

2008-04-10 00:00:00

pages

2466-77

issue

17

eissn

0950-9232

issn

1476-5594

pii

1210883

journal_volume

27

pub_type

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