Neural-cadherin expression associated with angiogenesis in non-small-cell lung cancer patients

Nakashima, Takashi; Huang, Cheng; Liu, D; Kameyama, Kotaro; Masuya, Daiki; Kobayashi, Shōji; Kinoshita, Moritoshi; Yokomise, Hiroyasu

doi:10.1038/sj.bjc.6600955

Cited by 42 publications

(38 citation statements)

References 34 publications

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“…It has been reported that the N-cadherin expression is uncommon in adenocarcinomas of the lung and is not a prognostic factor thereof (24,25). In the present study, incidences of N-cadherin expression were also low in poorly differentiated adenocarcinomas, as well as in epithelial and sarcomatous components of PCs.…”

Section: Discussionsupporting

confidence: 57%

Expression of adhesion molecules and transforming growth factor-β in pleomorphic carcinomas of the lung

et al. 2010

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Abstract. Pleomorphic carcinoma (PC) of the lung consists of an epithelial component showing the histology of poorly differentiated non-small cell carcinoma of the lung and a sarcomatous component, that is more aggressive compared to non-small cell carcinoma of the lung. To determine the differences between an epithelial component of PC and poorly differentiated non-small cell carcinoma, the expression of adhesion molecules (E-cadherin, β-catenin and N-cadherin) and transforming growth factor-β (TGF-β) was compared immunohistochemically among 14 poorly differentiated adenocarcinomas of the lung (PDAs) and 14 PCs of the lung, with an epithelial component, showing the histology of PDA. Expression levels of E-cadherin and β-catenin were significantly lower in epithelial or sarcomatous components of PCs than in PDAs while that of TGF-β was significantly higher in epithelial components of PCs than in PDAs. No significant difference was found in incidences of the expression of these molecules between epithelial and sarcomatous components of PCs. No significant difference was noted in the expression level of N-cadherin among PDAs and epithelial and sarcomatous components of PCs. The present results showed that E-cadherin and β-catenin expression is reduced and TGF-β expression is increased in epithelial components of PCs with the same histology as PDA when compared to PDAs, suggesting that an epithelial component of PC is distinct from non-small cell carcinoma with the same histology.

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Section: Discussionsupporting

confidence: 57%

Expression of adhesion molecules and transforming growth factor-β in pleomorphic carcinomas of the lung

et al. 2010

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“…Our previous studies revealed that tumour vascularity in NSCLCs is associated with intratumoral expression of VEGF-A (Masuya et al, 2001), interleukin-8 (Masuya et al, 2001, neuralcadherin (Nakashima et al, 2003), and that tumour vascularity is correlated with the survival rate of NSCLC patients (Nakashima et al, 2003). However, the present study did not show a correlation between the HGF/c-Met pathway and tumour vascularity in NSCLCs.…”

Section: Discussioncontrasting

confidence: 54%

The tumour–stromal interaction between intratumoral c-Met and stromal hepatocyte growth factor associated with tumour growth and prognosis in non-small-cell lung cancer patients

et al. 2004

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Immunohistochemical analyses of the effects of hepatocyte growth factor (HGF) and c-Met expression on tumour growth and angiogenesis were performed on 88 patients with non-small-cell lung cancers (NSCLCs). In all, 22 carcinomas (25.0%) were intratumoral HGF-positive, 14 carcinomas (15.9%) were stromal HGF-positive, and 36 carcinomas (40.9%) were intratumoral c-Metpositive. None of the carcinomas were stromal c-Met-positive. Examination of tumour growth revealed that the frequency of tumours with a high Ki-67 index was significantly greater for stromal HGF-positive tumours than for stromal HGF-negative tumours (P ¼ 0.0197). The frequency of tumours with a high Ki-67 index was also significantly greater for intratumoral c-Met-positive tumours than for intratumoral c-Met-negative tumours (P ¼ 0.0301). However, there was no significant difference in tumour vascularity with relation to intratumoral HGF status, stromal HGF status, and intratumoral c-Met status. The survival rate of patients with intratumoral c-Met-positive tumours was significantly lower than for patients with c-Met-negative tumours (P ¼ 0.0095). Furthermore, the survival rate of patients with both intratumoral c-Met-positive and stromal HGF-positive tumours was significantly lower than for patients with either positive tumours, and that of patients with both negative tumours (P ¼ 0.0183 and P ¼ 0.0011, respectively). A univariate analysis revealed that intratumoral c-Met expression was a significant prognostic factor of NSCLC patients (relative risk ¼ 2.642, P ¼ 0.0029). The present study demonstrates that tumour -stromal interaction between tumour cell-derived c-Met and stromal cellderived HGF affects tumour growth and the prognosis of NSCLC patients.

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“…Literature data demonstrated that N-cadherin is expressed during early neuroectoderm vascularization where it probably establishes interactions between neuroectoderm and endothelium, followed by a downregulation of N-cadherin in endothelia when the cells differentiate to a blood-retina and blood-brain barrier (Gerhardt et al, 1999). N-cadherin has also been indicated as an angiogenic factor in nonsmall-cell lung cancer because biopsies positive for N-cadherin were hypervascular (Nakashima et al, 2003). In our laboratory we could find that plasmin cleaved a 90 kD ectodomain fragment from N-cadherin, coined soluble N-cadherin.…”

Section: N-cadherin Function and Signallingmentioning

confidence: 99%

N-cadherin in the spotlight of cell-cell adhesion, differentiation, embryogenesis, invasion and signalling

Derycke

Bracke²

2004

Int. J. Dev. Biol.

361

284

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Cell migration is a process which is essential during embryonic development, throughout adult life and in some pathological conditions. Cadherins, and more specifically the neural cell adhesion molecule N-cadherin, play an important role in migration. In embryogenesis, N-cadherin is the key molecule during gastrulation and neural crest development. N-cadherin mediated contacts activate several pathways like Rho GTPases and function in tyrosine kinase signalling (for example via the fibroblast growth factor receptor). In cancer, cadherins control the balance between suppression and promotion of invasion. E-cadherin functions as an invasion suppressor and is downregulated in most carcinomas, while N-cadherin, as an invasion promoter, is frequently upregulated. Expression of N-cadherin in epithelial cells induces changes in morphology to a fibroblastic phenotype, rendering the cells more motile and invasive. However in some cancers, like osteosarcoma, N-cadherin may behave as a tumour suppressor. N-cadherin can have multiple functions: promoting adhesion or induction of migration dependent on the cellular context. KEY WORDS: N-cadherin, cancer, embryogenesis, invasion, signallingInt. J. Dev. Biol. 48: 463-476 (2004) Migration and invasionCell migration is a process that is essential during embryonic development and throughout further life. In the adult, cell migration is crucial for homeostatic processes, such as effective immune responses and repair of injured tissues. To migrate, the individual cell body must modify its shape to interact with the surrounding tissue structures. The extracellular matrix (ECM) forms a substrate, as well as a barrier for the advancing cell body. Cell migration through tissues results from a continuous cycle of interdependent steps. In general, there are five steps involved in cell migration in the ECM. First comes the protrusion of the leading edge, where growing actin filaments connect to adapter proteins and push the cell membrane in an outward direction. In a second step cell-matrix interactions and focal contacts are formed. After that, surface proteases such as matrix metalloproteinases (MMP) are recruited and focal proteolysis takes place. Then the cell contracts by actomyosin activation, and finally the tail of the cell is detached from its substrate (Friedl and Wolf, 2003).Border cells of the Drosophila melanogaster ovary are nowadays used as a model for migration. There are three recently discovered signalling pathways that control distinct aspects of migration: a global steroid-hormone signal defines the timing of migration, a highly localised cytokine signal that activates the Janus kinase-signal transducer and activator of transcription is both necessary and sufficient to induce migration, and finally, a growth factor that is analogous to platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) contributes to guiding the cells to their destination (Montell, 2003).In embryonic morphogenesis two types of collective cell movement can ...

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Neural-cadherin expression associated with angiogenesis in non-small-cell lung cancer patients

Cited by 42 publications

References 34 publications

Expression of adhesion molecules and transforming growth factor-β in pleomorphic carcinomas of the lung

Expression of adhesion molecules and transforming growth factor-β in pleomorphic carcinomas of the lung

The tumour–stromal interaction between intratumoral c-Met and stromal hepatocyte growth factor associated with tumour growth and prognosis in non-small-cell lung cancer patients

N-cadherin in the spotlight of cell-cell adhesion, differentiation, embryogenesis, invasion and signalling

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