N-cadherin switching occurs in high Gleason grade prostate cancer

Jaggi, Meena; Nazemi, Tanya M.; Abrahams, Neil A.; Baker, John J.; Galich, Anton; Smith, Lynette M.; Balaji, K.C.

doi:10.1002/pros.20334

Cited by 77 publications

(63 citation statements)

References 36 publications

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“…Whereas another calcium-dependent cell adhesion molecules, E-cadherin, is expressed in epithelial cells, N-cadherin is expressed in nerve system, skeletal muscle and mesenchymal cells (Jaggi et al, 2006). Recent evidence suggests that changes in cadherin expression or cadherin switching play a critical role during progression of various tumors including breast cancer (Hazan et al, 1997) and prostate cancer (Tomita et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

et al. 2007

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The androgen receptor (AR) plays a key role as a transcriptional factor in prostate development and carcinogenesis. Identification of androgen-regulated genes is essential to elucidate the AR pathophysiology in prostate cancer. Here, we identified androgen target genes that are directly regulated by AR in LNCaP cells, by combining chromatin immunoprecipitation (ChIP) with tiling microarrays (ChIP-chip). ChIP-enriched or control DNAs from the cells treated with R1881 were hybridized with the ENCODE array, in which a set of regions representing approximately 1% of the whole genome. We chose 10 bona fide AR-binding sites (ARBSs) (Po1e-5) and validated their significant AR recruitment ligand dependently. Eight upregulated genes by R1881 were identified in the vicinity of the ARBSs. Among the upregulated genes, we focused on UGT1A and CDH2 as AR target genes, because the ARBSs close to these genes (in UGT1A distal promoter and CDH2 intron 1) were most significantly associated with acetylated histone H3/H4, RNA polymerase II and p160 family co-activators. Luciferase reporter constructs including those two ARBSs exhibited ligand-dependent transcriptional regulator/enhancer activities. The present study would be powerful to extend our knowledge of the diversity of androgen genetic network and steroid action in prostate cancer cells.

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Section: Discussionmentioning

confidence: 99%

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

et al. 2007

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“…N-cadherin expression in prostate cancer is less well studied compared to E-cadherin expression. In one study, the switch of cadherin expression was associated with higher grade tumors (Jaggi et al 2006). In a total of 44 PC specimens 45% showed N-cadherin expression.…”

Section: N-cadherinmentioning

confidence: 96%

New experimental markers for early detection of high-risk prostate cancer: role of cell–cell adhesion and cell migration

Mól

Geldof

Meijer

et al. 2007

J Cancer Res Clin Oncol

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Today's treatment and diagnosis of prostate cancer still exhibit major limitations. The search for new and additional prognostic markers is therefore still an actual Weld of interest. Potential markers involved in numerous biological processes in the tumor cell have been investigated intensively. For therapeutic interventions it is important to distinguish between harmless and aggressive disease in an early stage. Therefore the subject of this review is limited to markers associated with those functional processes, which discriminate early stage aggressive, metastatic cancer from harmless disease. Important processes in this respect are: altered cell adhesion and cellular migration. E-cadherin, N-cadherin, -catenin, integrins, focal adhesion kinase, connexins and matrix metalloproteinases all appear promising biological markers associated with the early stage metastatic process in prostate cancer. Here we discuss their potential to become valid biological markers based on literature data. Thus far, none of these markers proved to be a valid individual marker by itself due to prostate cancer heterogeneity and transient expression. Analyzing a combination of the potential markers discussed in this review is expected to be a better approach toward discriminating high-from low-risk tumors in an early stage of prostate cancer.

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“…[14][15][16][17][18][19] Some studies have found an association between E-cadherin expression and prostate cancer grade or stage, while others have failed to do so; however, loss of E-cadherin and the onset of expression of N-cadherin are observed in high-grade prostate cancer. 17,[20][21][22] We previously found strong expression of cadherin-10 mRNA in human prostate. 23 The mRNA of this molecule is most strongly expressed in the central nervous system, 24 and we raised antiserum to show that the protein is present in blood-brain barrier capillaries, and in some ependymal epithelia, but not in nonbrain vessels.…”

mentioning

confidence: 96%

The intercellular adhesion molecule, cadherin-10, is a marker for human prostate luminal epithelial cells that is not expressed in prostate cancer

et al. 2008

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During the normal turnover of prostate epithelium, stem cells in the basal cell layer produce an intermediate cell population that gives rise to fully differentiated secretory luminal cells. This process is extensively studied in relation to the development of prostate disease, in particular, to elucidate the origin and nature of prostate cancer. We previously showed that the mRNA of a poorly characterised intercellular adhesion molecule, cadherin-10, is strongly expressed in human prostate. Using anticadherin-10 antibodies, immunohistochemistry, and confocal microscopy, we have examined the pattern of cadherin-10 expression in relation to human prostate epithelial differentiation markers (E-cadherin, CD44, and cytokeratins (CK) 14, 18 and 19) in archival paraffin-embedded and fixed-frozen histopathological specimens in individual and serial sections. In nonneoplastic prostate, E-cadherin is expressed by all basal and luminal epithelial cells, while cadherin-10 is variably expressed in luminal cells where it is colocalised with E-cadherin at basolateral plasma membranes. Cadherin-10 is absent in CK14-and/or CD44-positive basal cells, but is expressed in CK18-positive luminal cells (differentiated secretory cells), a subset of CK19-positive intermediate/luminal cells, but not CK19-positive basal cells. Small foci of prostate cancer express E-cadherin, CK19 and CK18, but cadherin-10 expression is low or undetectable. These findings suggest that the expression of cadherin-10 is associated with the later stages of differentiation of luminal secretory cells, indicating a specific role in secretory cell terminal differentiation. While prostate cancer cells express secretory cell markers (eg, CK18, prostate-specific antigen) and the more generally expressed E-cadherin, their failure to express cadherin-10 further emphasises a role for this cadherin in normal prostate organisation and function.

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N-cadherin switching occurs in high Gleason grade prostate cancer

Abstract: We have demonstrated for the first time that N-cadherin switching occurs in higher grade PC and correlates significantly with increasing Gleason patterns. N-cadherin may be as a useful biomarker of aggressive PC.

Cited by 77 publications

References 36 publications

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

Identification of novel androgen response genes in prostate cancer cells by coupling chromatin immunoprecipitation and genomic microarray analysis

New experimental markers for early detection of high-risk prostate cancer: role of cell–cell adhesion and cell migration

The intercellular adhesion molecule, cadherin-10, is a marker for human prostate luminal epithelial cells that is not expressed in prostate cancer

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