Embryonic expression of epithelial membrane protein 1 in early neurons

Wulf, Philip; Suter, Ueli

doi:10.1016/s0165-3806(99)00092-9

Cited by 38 publications

(20 citation statements)

References 59 publications

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“…The results of the immunohistochemistry staining proved that the abnormal expression of EMP1 was seen in epilepsy group, but not seen in the normal control group. They were the same as the earlier research; the earlier research found EMP1 was seen in the immature mouse brain, but lost in the adult [18]. In human tissues, EMP1 mRNA was not detected in brain [11].…”

Section: Discussionsupporting

confidence: 83%

Up-Regulation of Epithelial Membrane Protein-1 in the Temporal Neocortex of Patients with Intractable Epilepsy

Xue

Wang

et al. 2009

Neurochem Res

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Epithelial membrane protein-1 (EMP-1), called Tumor-associated membrane protein, is the marker of a drug-resistant tumor and take part in the drug-resistant mechanism of tumor, with the relationship of epidermal growth factor receptor (EGFR). Because there are some similarities between the pathogenesis and the drug resistance mechanism of tumor and the drug resistance mechanisms in epilepsy. EMP1 expression may be connected with the drug-resistance mechanism of epilepsy. We detected EMP-1 by gene scanning and immunohistochemistry staining, comparing the IE group and the control group, and we investigated the relationship between EMP-1 and EGFR by double-label immunofluorescence staining in the IE group. We found expression of EMP-1 mRNA was higher in IE per the gene scanning, EMP-1 immunoreactivity was apparent in neurons of IE patients but not in the control group, and the expression of EMP-1 and EGFR occurred in the same neuron. We confirm EMP-1 is abnormally expressed in IE and suggest the interaction of EGFR and EMP-1 plays a role in the mechanism of drug resistance in epilepsy and may be a new gene for drug resistance.

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Section: Discussionsupporting

confidence: 83%

Up-Regulation of Epithelial Membrane Protein-1 in the Temporal Neocortex of Patients with Intractable Epilepsy

Xue

Wang

et al. 2009

Neurochem Res

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“…EMP1, alternatively referred to as tumor-associated membrane protein, has been detected in embryonic kidney, brain, gut and is linked to cell-cell interactions and the regulation of cell proliferation, in addition to neuronal differentiation and neurite outgrowth [48][49][50]. Similarly, the induced expression of keratin 7, indicative of a simple epithelial cell type, in the mesenchymally-derived poorly aggressive melanoma cells, strongly suggests their transition to a dedifferentiated, interconverted phenotype, previously shown by our laboratory and others to be closely associated with aggressive behavior and metastatic disease [26,[51][52][53].…”

Section: Discussionmentioning

confidence: 99%

The epigenetic reprogramming of poorly aggressive melanoma cells by a metastatic microenvironment

Seftor¹,

Meltzer²,

Kirschmann³

et al. 2006

J Cellular Molecular Medi

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Cancer pathogenesis involves dynamic interactions within the tumor-host microenvironment. Most noteworthy is cutaneous melanoma which is considered one of the few remaining cancers escalating in incidence [1,2], and thus represents a growing public health burden worldwide [3; for review, see 4; 5]. In addition, uveal melanoma is considered the most common primary intraocular cancer in adults [6], where metastasis occurs in an unpredictable manner in approximately 50% of patients with a primary tumor originating in the choroid or ciliary body of the eye [6]. Without question, the clinical manage- AbstractA dynamic, complex relationship exists between tumor cells and their microenvironment, which plays a pivotal role in cancer progression, yet remains poorly understood. Particularly perplexing is the finding that aggressive melanoma cells express genes associated with multiple cellular phenotypes, in addition to their ability to form vasculogenic-like networks in three-dimensional matrix -called vasculogenic mimicry, which is illustrative of tumor cell plasticity. This study addressed the unique epigenetic effect of the microenvironment of aggressive melanoma cells on the behavior of poorly aggressive melanoma cells exposed to it. The data show significant changes in the global gene expression of the cells exposed to 3-D matrices preconditioned by aggressive melanoma cells, including the acquisition of a vasculogenic cell phenotype, upregulation of ECM remodeling genes, and increased invasive ability -indicative of an epigenetic, microenvironment-induced reprogramming of poorly aggressive melanoma cells. However, this epigenetic effect was completely abrogated when a highly cross-linked collagen matrix was used, which could not be remodeled by the aggressive melanoma cells. These findings offer an unique perspective of the inductive properties associated with an aggressive melanoma microenvironment that might provide new insights into the epigenetic regulation of tumor cell plasticity and differentiation, as well as mechanisms that could be targeted for novel therapeutic strategies.

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“…Although the highest expression levels are found in myelin-forming Schwann cells, PMP22 mRNA can be detected in a multitude of developing and mature nonneural tissues, including epithelia of the intestine (Baechner et al, 1995;Taylor et al, 1995;Wulf and Suter, 1999) and the choroid plexus (Roux et al, 2004). The specific role of PMP22 in Schwann cells remains undefined, although it is known that altered expression is associated with heritable demyelinating peripheral neuropathies (Naef and Suter, 1998).…”

Section: Introductionmentioning

confidence: 99%

Modulation of Epithelial Morphology, Monolayer Permeability, and Cell Migration by Growth Arrest Specific 3/Peripheral Myelin Protein 22

Roux

Amici

Fletcher

et al. 2005

MBoC

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Peripheral myelin protein 22 (PMP22) is associated with a subset of hereditary peripheral neuropathies. Although predominantly recognized as a transmembrane constituent of peripheral nerve myelin, PMP22 is localized to epithelial and endothelial cell-cell junctions, where its function remains unknown. In this report, we investigated the role of PMP22 in epithelial biology. Expression of human PMP22 (hPMP22) slows cell growth and induces a flattened morphology in Madin-Darby canine kidney (MDCK) cells. The transepithelial electrical resistance (TER) and paracellular flux of MDCK monolayers are elevated by hPMP22 expression. After calcium switch, peptides corresponding to the second, but not the first, extracellular loop of PMP22 perturb the recovery of TER and paracellular flux. Finally, subsequent to wounding, epithelial monolayers expressing hPMP22 fail to migrate normally. These results indicate that PMP22 is capable of modulating several aspects of epithelial cell biology, including junctional permeability and wound closure. INTRODUCTIONThe tetraspan glycoprotein peripheral myelin protein 22 (PMP22), also known as growth arrest specific 3 (gas3) gene, has proposed roles in peripheral nerve myelin formation, cell-cell interactions, and cell proliferation (Suter and Snipes, 1995). Although the highest expression levels are found in myelin-forming Schwann cells, PMP22 mRNA can be detected in a multitude of developing and mature nonneural tissues, including epithelia of the intestine (Baechner et al., 1995;Taylor et al., 1995;Wulf and Suter, 1999) and the choroid plexus (Roux et al., 2004). The specific role of PMP22 in Schwann cells remains undefined, although it is known that altered expression is associated with heritable demyelinating peripheral neuropathies (Naef and Suter, 1998). Similarly, the function of the protein at nonneural locations remains undetermined.In vitro studies have identified a role for PMP22 in the regulation of cell proliferation and morphology. In Schwann cells, elevated expression delays the transition from G0/G1 to the S phase of the cell cycle (Zoidl et al., 1995), and can lead to apoptosis in some instances (Fabbretti et al., 1995;Zoidl et al., 1997). Conversely, reduced PMP22 mRNA levels are associated with enhanced DNA synthesis and entry into the S ϩ G2/M phases (Zoidl et al., 1995). In NIH 3T3 fibroblasts, PMP22 overexpression regulates cell spreading, an effect that is dependent on the Rho-GTPase pathway (Brancolini et al., 1999). Recent studies have detected exogenous PMP22 in ADP-ribosylation factor 6 (Arf-6)-positive plasma membrane-endosomal recycling vacuoles before apoptosis or changes in cell shape (Chies et al., 2003). This pathway is known to be involved in modulating the actin cytoskeleton, cell polarity, adhesion, and migration (Donaldson, 2003). Together, these findings support the notion that PMP22 has a significant role in basic cellular processes, extending beyond an involvement in Schwann cell myelination.We previously described PMP22 as a constituent of apical ...

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Embryonic expression of epithelial membrane protein 1 in early neurons

Cited by 38 publications

References 59 publications

Up-Regulation of Epithelial Membrane Protein-1 in the Temporal Neocortex of Patients with Intractable Epilepsy

Up-Regulation of Epithelial Membrane Protein-1 in the Temporal Neocortex of Patients with Intractable Epilepsy

The epigenetic reprogramming of poorly aggressive melanoma cells by a metastatic microenvironment

Modulation of Epithelial Morphology, Monolayer Permeability, and Cell Migration by Growth Arrest Specific 3/Peripheral Myelin Protein 22

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