Annexins as cell-type-specific markers in the developing chicken chorionallantoic membrane

Matschke, Katharina; Silva-Azevedo, Luis Da; Hlushchuk, Ruslan; Djonov, Valentin; Baum, Oliver

doi:10.1007/s00441-005-0112-1

Cited by 18 publications

(21 citation statements)

References 34 publications

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“…The upper chorionic epithelium is heavily vascularized by BM-encased capillaries and subtended by a continuous epithelial-derived BM that demarcates the epithelium from the underlying mesenchyme ( Fig. 1 A) (10). Immunohistochemical staining with chick type IV collagen-specific antibodies clearly identifies (i) capillary BMs interspersed within the chorionic epithelium, (ii) the upper chorionic and lower allantoic epithelial BMs, and (iii) the vascular BMs surrounding arterioles and venules that traverse the CAM mesenchyme (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…To define cancer cell-BM interactions in an in vivo setting, neoplastic cell populations were cultured atop the CAM, an extra-embryonic tissue consisting of a chorionic epithelium of ectodermal origin, an intermediate mesenchyme and an endodermal allantoic epithelium (Fig. 1A) (10). The upper chorionic epithelium is heavily vascularized by BM-encased capillaries and subtended by a continuous epithelial-derived BM that demarcates the epithelium from the underlying mesenchyme ( Fig.…”

Section: Resultsmentioning

confidence: 99%

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Induction of a MT1-MMP and MT2-MMP-dependent basement membrane transmigration program in cancer cells by Snail1

Ota

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

186

176

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EMT ͉ extracellular matrix ͉ Snail T he transition of carcinoma in situ to a frankly carcinomatous lesion requires the cancer cells to acquire an ability to perforate and transmigrate the underlying basement membrane (BM), a specialized form of extracellular matrix (ECM) that subtends all epithelial cells (1, 2). Current evidence suggests that the induction of a BM-invasive phenotype may be linked to the expression of zinc-finger transcriptional repressors capable of promoting an epithelial-mesenchymal cell transition (EMT) which trigger epithelial cell-derived cancer cells to adopt a tissue-invasive, mesenchymal cell-like phenotype (2-4). Snail1 is a prototypical member of a family of EMT-inducing transcription factors, playing a required role in developmental programs, such as gastrulation, and capable of undergoing pathologic re-activation postnatally in neoplastic states (5). While Snail1 has been linked to cancer cell invasion programs, cancer recurrence, and the adoption of cancer stem cell-like properties (2, 5), the mechanisms by which the transcription factor induces BM degradation and invasion programs remain undefined.Recent efforts to delineate normal or neoplastic cell interactions with the intact BM in an in vivo setting have been limited largely to model organisms where changes in BM structure during invasive processes can be evaluated directly by microscopic imaging (6, 7). In vertebrate systems, experimental models are unavailable where carcinoma cells can be situated atop linear, unbroken stretches of BM and invasion monitored in a fashion that lends itself to molecular characterization in vivo. Herein, we have adopted a live chick chorioallantoic membrane (CAM) model to analyze the cancer cell-BM interactions that underlie the earliest steps in the carcinoma invasion program (3, 4, 8, 9). These studies demonstrate that Snail1 induces cancer cells to transmigrate BM barriers by mobilizing the membrane-type matrix metalloproteinases (MTMMPs), MT1-MMP and MT2-MMP (1). Working in tandem, these MT-MMP family members not only confer carcinoma cells with the ability to perforate BM structures in vivo, but also to trigger angiogenesis, cancer cell proliferation and dissemination of the transformed cells to distant sites through the host vasculature. These findings suggest that Snail1, and perhaps all EMT-inducing transcription factors, mobilize MT1-MMP and/or MT2-MMP as necessary co-factors during tumor progression. ResultsSnail1-Induced BM Degradation and Transmigration by Breast Carcinoma Cells. To define cancer cell-BM interactions in an in vivo setting, neoplastic cell populations were cultured atop the CAM, an extra-embryonic tissue consisting of a chorionic epithelium of ectodermal origin, an intermediate mesenchyme and an endodermal allantoic epithelium (Fig. 1A) (10). The upper chorionic epithelium is heavily vascularized by BM-encased capillaries and subtended by a continuous epithelial-derived BM that demarcates the epithelium from the underlying mesenchyme (Fig.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Induction of a MT1-MMP and MT2-MMP-dependent basement membrane transmigration program in cancer cells by Snail1

Ota

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

186

176

View full text Add to dashboard Cite

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“…They were post-fixed in 1% OsO 4 (0.1 M sodium-cacodylate, pH 7.4, 340 mOsm), dehydrated in ethanol and embedded in Epon 812 (Fluka, Buchs, Switzerland). Semi-thin sections were prepared, stained with toluidine blue, and analysed with a light microscope6667. Representative areas were selected and further imaged by transmission electron microscopy.…”

Section: Methodsmentioning

confidence: 99%

Structural decoding of netrin-4 reveals a regulatory function towards mature basement membranes

et al. 2016

Self Cite

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Netrins, a family of laminin-related molecules, have been proposed to act as guidance cues either during nervous system development or the establishment of the vascular system. This was clearly demonstrated for netrin-1 via its interaction with the receptors DCC and UNC5s. However, mainly based on shared homologies with netrin-1, netrin-4 was also proposed to play a role in neuronal outgrowth and developmental/pathological angiogenesis via interactions with netrin-1 receptors. Here, we present the high-resolution structure of netrin-4, which shows unique features in comparison with netrin-1, and show that it does not bind directly to any of the known netrin-1 receptors. We show that netrin-4 disrupts laminin networks and basement membranes (BMs) through high-affinity binding to the laminin γ1 chain. We hypothesize that this laminin-related function is essential for the previously described effects on axon growth promotion and angiogenesis. Our study unveils netrin-4 as a non-enzymatic extracellular matrix protein actively disrupting pre-existing BMs.

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“…The CAM consists of surface chorionic epithelium separated by connective tissue from the endodermal allantoic membrane (19–20). The chorionic epithelium is separated from the underlying connective tissue by an intact epithelial-derived BM that contains type IV collagen (19).…”

Section: Methodsmentioning

confidence: 99%

Inactivation or Loss of TTP Promotes Invasion in Head and Neck Cancer via Transcript Stabilization and Secretion of MMP9, MMP2, and IL-6

Tubergen

Banerjee

Liu

et al. 2013

Clinical Cancer Research

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Purpose Invasion is the critical step in progression of a pre-cancerous lesion to squamous cell carcinoma of the head and neck (SCCHN). Invasion is regulated by multiple pro-inflammatory mediators. Tristetraprolin (TTP) is an mRNA degrading protein that regulates multiple pro-inflammatory mediators. TTP may serve as an excellent treatment target. Rap1 is a ras-like oncoprotein that induces critical signaling pathways. In this study, the role of rap1 in TTP-mediated invasion was investigated. Experimental Design Using complementary approaches we modulated TTP and altered expression of IL-6 and MMP2/9, which were quantified by ELISA and zymogram. Invasion was evaluated in vitro using the Oral-Cancer-Equivalent (OCE) 3D model and in vivo in the chick chorioallantoic membrane (CAM). The role of rap1 and p38 were established using knockdown strategies. Results Downregulation of TTP significantly increased invasion via secretion of MMP9/2 and IL-6. In the novel OCE and CAM invasion models of SCCHN, cells with downregulated TTP destroyed the basement membrane to invade the underlying connective tissue. Rap1 induces p38 mitogen activated protein kinase (p38)-mediated inactivation of TTP. Inactive TTP enhances transcript stability via binding to the 3′-UTR. High IL-6 and MMP9 are prognostic for poor clinical outcomes in SCCHN patients. Conclusions Targeting the rap1-p38-TTP cascade is an attractive novel treatment strategy in SCCHN to concurrently suppress multiple mediators of invasion.

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Annexins as cell-type-specific markers in the developing chicken chorionallantoic membrane

Cited by 18 publications

References 34 publications

Induction of a MT1-MMP and MT2-MMP-dependent basement membrane transmigration program in cancer cells by Snail1

Induction of a MT1-MMP and MT2-MMP-dependent basement membrane transmigration program in cancer cells by Snail1

Structural decoding of netrin-4 reveals a regulatory function towards mature basement membranes

Inactivation or Loss of TTP Promotes Invasion in Head and Neck Cancer via Transcript Stabilization and Secretion of MMP9, MMP2, and IL-6

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