Cell Adhesion Molecule CEACAM1 Associates with Paxillin in Granulocytes and Epithelial and Endothelial Cells

Ebrahimnejad, Alireza; Flayeh, Raid; Unteregger, Gerhard; Wagener, Christoph; Brümmer, Jens

doi:10.1006/excr.2000.5026

Cited by 31 publications

(29 citation statements)

References 31 publications

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“…44 -46 In granulocytes and endothelial cells, CEACAM1 associates with talin, a major cytoskeletal protein implicated in integrin activation. 40,47 Recently, osteopontin, a secreted ECM glycoprotein, and CEACAM1 were suggested to act as a functional complex to enhance invasiveness of trophoblast cells. 48 Thus, CEACAM1 is able to interact and interfere with integrins or integrin-regulated cellular functions and therefore to affect the cellular interactions with the ECM.…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Hormone Modulates Human Trophoblast Invasion through Carcinoembryonic Antigen-Related Cell Adhesion Molecule-1 Regulation

Bamberger

Minas

Kalantaridou

et al. 2006

The American Journal of Pathology

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Abnormalities in the process of trophoblast invasion may result in abnormal placentation. Both the embryonic trophoblast and maternal decidua produce corticotropin-releasing hormone (CRH), which promotes implantation. Carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1), which is expressed in extravillous trophoblasts (EVTs) of normal human placenta, may also function in trophoblast/endometrial interactions. We investigated whether locally produced CRH plays a role in trophoblast invasion, primarily by regulating CEACAM1 expression. We examined cultures of freshly isolated human EVTs, which express CEACAM1, and an EVTbased hybridoma cell line, which is devoid of endogenous CEACAM1. CRH inhibited EVT invasion in Matrigel invasion assays, and this effect was blocked by the CRH receptor type 1 (CRHR1)-specific antagonist antalarmin. Additionally, CRH decreased CEACAM1 expression in EVTs in a dose-dependent manner. After transfection of the hybridoma cell line with a CEACAM1 expression vector, the invasiveness of these cells was strongly enhanced. This effect was inhibited by addition of blocking monoclonal antibody against CEACAM1. Furthermore, blocking of endogenous CEACAM1 in EVTs inhibited the invasive potential of these cells. Taken together these findings suggest that CRH inhibits trophoblast invasion by decreasing the expression of CEACAM1 through CRHR1, an effect that might be involved in the pathophysiology of clinical conditions, such as preeclampsia and placenta accreta. The complex developmental process of implantation involves a series of steps leading to an effective cross-talk between invasive trophoblast cells and the maternal endometrium. This dynamic process requires a precisely coordinated development of a hormonally primed adhesive endometrium and a blastocyst competent to implant. The trophoblast undergoes a number of distinct interactions with the underlying endometrial surface initiated by apposition, which involves close proximity between trophoblast and endometrial epithelium, followed by attachment, and concluded by invasion of trophoblast into the decidualized stroma.1 However, the molecular interactions at the embryo-maternal interface during the time of adhesion and subsequent invasion are not fully understood.The hypothalamic neuropeptide corticotropin-releasing hormone (CRH) is produced in several organs of the female reproductive system, including the endometrial glands, decidualized stroma, and trophoblast. [2][3][4][5][6] In addition, the gene encoding the CRH receptor type 1Supported by the Alexander Onassis Foundation (grant to A.M. and S.N.K.) and the Deutsche Krebshilfe (grant 10-2063 to A.M.B. and J.B.).

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Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Hormone Modulates Human Trophoblast Invasion through Carcinoembryonic Antigen-Related Cell Adhesion Molecule-1 Regulation

Bamberger

Minas

Kalantaridou

et al. 2006

The American Journal of Pathology

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“…45,47,[51][52][53][54][55] Moreover, CEA-CAM1, like BCR/ABL, has been shown to associate with the actin cytoskeleton, possible by interacting with paxillin. [56][57][58][59][60] In the hematopoietic system no detailed studies on the expression of CEACAM1 in different cellular compartments are available, but during normal hematopoiesis the expression pattern of the CEACAM1, CEACAM6 and CEACAM8 molecules has been shown to change with different maturation stages, first appearing at the promyelocytic stage and then showing increased expression on myelocytes and metamyelocytes. 61,62 An interesting observation in this context is that CEAs have been shown to be aberrantly expressed in ALL, preferentially in Philadelphia (Ph)-positive cases.…”

Section: Discussionmentioning

confidence: 99%

Establishment and phenotypic characterization of human U937 cells with inducible P210 BCR/ABL expression reveals upregulation of CEACAM1 (CD66a)

et al. 2004

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“…It was shown that CEACAM1 expression varies in proliferating and quiescent epithelial cells and that this influences their proliferation (13). The colocalization and interaction of CEACAM1 with paxillin and integrin ␤ (3) recently were shown (14,15).…”

Section: Introductionmentioning

confidence: 98%

Dual Role of Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 in Angiogenesis and Invasion of Human Urinary Bladder Cancer

Oliveira‐Ferrer

Tilki²,

Ziegeler³

et al. 2004

Cancer Research

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Here, we show that carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) is expressed in umbrella cells of bladder urothelium but is down-regulated in superficial bladder cancer, such as histologic tumor stage a (pTa) and transitional cell carcinoma in situ (pTis). Concurrently, CEACAM1 is up-regulated in the endothelia of adjacent angiogenic blood vessels. Mimicking the CEACAM1 down-regulation in the urothelium, CEACAM1 was silenced in bladder cancer cell lines 486p and RT4 using the small interfering RNA technique. CEACAM1 downregulation was confirmed at the protein level by Western blot analyses. CEACAM1 silencing leads to a significant up-regulation of vascular endothelial growth factor (VEGF)-C and VEGF-D in quantitative reverse transcription-PCR. Correspondingly, supernatants from the CEACAM1-overexpressing bladder cancer cell lines reduce, but those from CEACAM1 silencing induce endothelial tube formation and potentiate the morphogenetic effects of VEGF. These data suggest that the epithelial down-regulation of CEACAM1 induces angiogenesis via increased expression of VEGF-C and VEGF-D. Inversely, CEACAM1 is up-regulated in endothelial cells of angiogenic blood vessels. This in turn is involved in the switch from noninvasive and nonvascularized to invasive and vascularized bladder cancer. CEACAM1 appears to be a promising endothelial target for bladder cancer therapy.

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Cell Adhesion Molecule CEACAM1 Associates with Paxillin in Granulocytes and Epithelial and Endothelial Cells

Cited by 31 publications

References 31 publications

Corticotropin-Releasing Hormone Modulates Human Trophoblast Invasion through Carcinoembryonic Antigen-Related Cell Adhesion Molecule-1 Regulation

Corticotropin-Releasing Hormone Modulates Human Trophoblast Invasion through Carcinoembryonic Antigen-Related Cell Adhesion Molecule-1 Regulation

Establishment and phenotypic characterization of human U937 cells with inducible P210 BCR/ABL expression reveals upregulation of CEACAM1 (CD66a)

Dual Role of Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 in Angiogenesis and Invasion of Human Urinary Bladder Cancer

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