Novel expression of N-cadherin elicits in vitro bladder cell invasion via the Akt signaling pathway

Rieger-Christ, Kimberly; Lee, Peter; Zagha, Ralph M.; Kosakowski, Monika; Moinzadeh, Alireza; Stoffel, John T.; Ben-Ze’ev, Avri; Libertino, John A.; Summerhayes, Ian C.

doi:10.1038/sj.onc.1207629

Cited by 69 publications

(56 citation statements)

References 34 publications

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“…Electron microscopies or image-directed Doppler sonography of autonomous adenomas are compatible with such a picture (Dralle and Bocker, 1977;Becker et al, 1997). The increased expression of N-cadherin in autonomous adenomas which do not metastasize and which rarely evolve to carcinomas is a strong argument against the concept of N-cadherin as a marker for tumor cell invasion and metastasis (Rieger-Christ et al, 2004). It would rather facilitate direct interaction of tumor and endothelial cells, which would lead to the capillarization of the autonomous adenomas, but could also be a primary step in the penetration of cancer cells in the vascular lumen.…”

Section: Discussionmentioning

confidence: 95%

Gene expression in thyroid autonomous adenomas provides insight into their physiopathology

Wattel¹,

Mircescu²,

Venet³

et al. 2005

Oncogene

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The purpose of this study was to use the microarray technology to define expression profiles characteristic of thyroid autonomous adenomas and relate these findings to physiological mechanisms. Experiments were performed on a series of separated adenomas and their normal counterparts on Micromax cDNA microarrays covering 2400 genes (analysis I), and on a pool of adenomatous tissues and their corresponding normal counterparts using microarrays of 18 000 spots (analysis II). Results for genes present on the two arrays corroborated and several gene regulations previously determined by Northern blotting or microarrays in similar lesions were confirmed. Five overexpressed and 24 underexpressed genes were also confirmed by real-time RT-PCR in some of the samples used for microarray analysis, and in additional tumor specimens. Our results show: (1) a change in the cell populations of the tumor, with a marked decrease in lymphocytes and blood cells and an increase in endothelial cells. The latter increase would correspond to the establishment of a close relation between thyrocytes and endothelial cells and is related to increased N-cadherin expression. It explains the increased blood flow in the tumor; (2) a homogeneity of tumor samples correlating with their common physiopathological mechanism: the constitutive activation of the thyrotropin (TSH)/cAMP cascade; (3) a low proportion of regulated genes consistent with the concept of a minimal deviation tumor; (4) a higher expression of genes coding for specific functional proteins, consistent with the functional hyperactivity of the tumors; (5) an increase of phosphodiesterase gene expression which explains the relatively low cyclic AMP levels measured in these tumors; (6) an overexpression of antiapoptotic genes and underexpression of proapoptotic genes compatible with their low apoptosis rate; (7) an overexpression of N-cadherin and downregulation of caveolins, which casts doubt about the use of these expressions as markers for malignancy.Oncogene (2005) 24, 6902-6916.

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Section: Discussionmentioning

confidence: 95%

Gene expression in thyroid autonomous adenomas provides insight into their physiopathology

Wattel¹,

Mircescu²,

Venet³

et al. 2005

Oncogene

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“…Thus, N-cadherin on FLS may influence FGFR signaling, thereby regulating FLS activation and proliferation. Lastly, N-cadherin activates the PI-3 kinase/Akt pathway, leading to enhanced expression of antiapoptotic factors such as Bcl-2 (39). Taken together, these alterations could contribute to the synovial lining hyperplasia noted in RA.…”

Section: Discussionmentioning

confidence: 98%

Coexpression of two mesenchymal cadherins, cadherin 11 and N‐cadherin, on murine fibroblast‐like synoviocytes

Agarwal

Lee

Kiener

et al. 2008

Arthritis & Rheumatism

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Objective. Cadherin 11 has recently been identified on fibroblast-like synoviocytes (FLS), and studies in mice have demonstrated its importance in synovial lining architecture and inflammation. However, many tissues express more than 1 cadherin. Given the newly appreciated functional significance of cadherins in the synovium, this study was undertaken to determine whether mouse FLS express other cadherins in addition to cadherin 11.Methods. The characterization of cadherin expression was determined in FLS derived from wild-type and cadherin 11-null mice using immunofluorescence (IF), biochemical, and immunohistologic techniques.Results. Cadherin 11 expression was observed at points of cell-cell contact in cultured wild-type mouse FLS. However, despite the lack of cell surface cadherin 11, cadherin 11-null mouse FLS cells still formed intimate cell-cell contacts that contained ␤-catenin. Immunoprecipitation of cell surface biotinylated FLS with anti-␤-catenin antibody demonstrated the presence of 2 cell surface catenin-associated proteins in FLS from wild-type mice and 1 in FLS sample from cadherin 11-null mice. Using biochemical approaches and reverse transcriptase-polymerase chain reaction, these proteins were determined to be N-cadherin and cadherin 11. Expression of both N-cadherin and cadherin 11 in the synovial lining was demonstrated by immunohistochemical analysis of mouse synovium. IF analyses demonstrated colocalization of N-cadherin and cadherin 11 to the same points of cell-cell contact. However, the inability to coimmunoprecipitate both cadherins using either anti-N-cadherin or anti-cadherin 11 antibodies suggests that these cadherins are not contained within the same molecular complexes.Conclusion. These findings demonstrate that FLS express both N-cadherin and cadherin 11, and suggest that these cadherins are not contained within the same molecular complex. Given their importance in modulating cellular behavior, understanding how these cadherins regulate FLS behavior individually and in concert will be critical to understanding synovial architecture and inflammation.

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“…8A). We found that these concentrations of inhibitors are not toxic to the cells by trypan blue staining and, on the other hand, they are being used in other studies (37)(38)(39)(40). PU5-1.8 cells were cultured for 2 h in media containing these inhibitors, and then cells were stimulated with Ep1.B peptide.…”

Section: Ep1b Activates Pi3k and Mapk Signaling Pathwaysmentioning

confidence: 96%

Dendritic Cell Differentiation Induced by a Self-Peptide Derived from Apolipoprotein E

Stephens

Nikoopour

Rider

et al. 2008

The Journal of Immunology

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Dendritic cells (DCs) are professional APCs and potent stimulators of naive T cells. Since DCs have the ability to immunize or tolerize T cells they are unique candidates for use in immunotherapy. Our laboratory has discovered that a naturally processed self-peptide from apolipoprotein E, Ep1.B, induces DC-like morphology and surface marker expression in a murine monocytic cell line (PU5-1.8), human monocytic cell line (U937), murine splenocytes, and human peripheral blood monocytes. Microscopy and flow cytometric analysis revealed that Ep1.B-treated cells display decreased adherence to plastic and increased aggregation, dendritic processes, and expression of DC surface markers, including DEC-205, CD11c, B7.1, and B7.2. These effects were observed in both PU5-1.8 cells and splenocytes from various mouse strains including BALB/c, C57BL/6, NOD/Lt, and C3H/HeJ. Coadministration of Ep1.B with OVA antigenic peptide functions in dampening specific immune response to OVA. Ep1.B down-regulates proliferation of T cells and IFN-γ production and stimulates IL-10 secretion in immunized mice. Ep1.B-induced differentiation resulted in the activation of PI3K and MAPK signaling pathways, including ERK1/2, p38, and JNK. We also found that NF-κB, a transcription factor essential for DC differentiation, is critical in mediating the effects of Ep1.B. Ep1.B-induced differentiation is independent of MyD88-dependent pathway of TLR signaling. Cumulatively, these findings suggest that Ep1.B acts by initiating a signal transduction cascade in monocytes leading to their differentiation into DCs.

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Novel expression of N-cadherin elicits in vitro bladder cell invasion via the Akt signaling pathway

Cited by 69 publications

References 34 publications

Gene expression in thyroid autonomous adenomas provides insight into their physiopathology

Gene expression in thyroid autonomous adenomas provides insight into their physiopathology

Coexpression of two mesenchymal cadherins, cadherin 11 and N‐cadherin, on murine fibroblast‐like synoviocytes

Dendritic Cell Differentiation Induced by a Self-Peptide Derived from Apolipoprotein E

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