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

Mól, Anna; Geldof, Albert A.; Meijer, Gerrit A.; Poel, Henk G. van der; Moorselaar, R. Jeroen A. van

doi:10.1007/s00432-007-0235-8

Cited by 34 publications

(23 citation statements)

References 35 publications

(36 reference statements)

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“…Cell adhesion is a significant process in cancer (18). The steroid biosynthesis pathway was found to be active between the castrated and benign tissue, as expected.…”

Section: Discussionmentioning

confidence: 99%

Identification of androgen-regulated genes in human prostate

Vaarala

Hirvikoski

Kauppila

et al. 2012

Molecular Medicine Reports

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Androgens are essential for the development of the prostate and prostate cancer. We examined androgen-regulated gene expression in the human prostate. Samples from benign and malignant prostate tissue and samples containing prostate tissue obtained from prostate cancer patients three days after surgical castration were further processed as probes for a GeneChip array. The comparison of gene expression profiles in castrated samples and in benign or malignant prostate tissue samples revealed androgen-regulated genes. We further evaluated the genes which were differentially expressed in benign and malignant prostate samples. The androgen-regulated expression of dual specificity phosphatase 1 (DUSP1) was confirmed in the LNCaP prostate cancer cell line, as the expression of DUSP1 increased with androgen treatment over the course of time. The expression of the genes CRISP3, PCA3, OR51E2, HOXC6, AGR3, AMACR and SLC14A1 was affected by castration in addition to differential expression in the benign and malignant prostate. These sample results require further investigation for the role of AGR3 and SLC14A1 in prostate cancer as these associations have not been reported previously.

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“…Cell adhesion is a significant process in cancer (18). The steroid biosynthesis pathway was found to be active between the castrated and benign tissue, as expected.…”

Section: Discussionmentioning

confidence: 99%

Identification of androgen-regulated genes in human prostate

Vaarala

Hirvikoski

Kauppila

et al. 2012

Molecular Medicine Reports

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“…The resulting mesenchymal-like phenotype is suitable for tumor invasion and dissemination, allowing metastatic progression to proceed (Becker et al, 2007;Guarino et al, 2007). Decrease or loss of expression of E-cadherin is often reported as an early event in the development of many tumors, such as gastric cancer (Graziano et al, 2003;Yi Kim et al, 2007), breast carcinoma cell lines (Lombaerts et al, 2006) and prostate cancer (Mol et al, 2007).…”

Section: Introductionmentioning

confidence: 99%

Differential expression of E-cadherin gene in human neuroepithelial tumors

Motta¹,

Valera²,

Lucio-Eterovic³

et al. 2008

Genet. Mol. Res.

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ABSTRACT. Cadherins are cell-to-cell adhesion molecules that play an important role in the establishment of adherent-type junctions by mediating calcium-dependent cellular interactions. The CDH1 gene encodes the transmembrane glycoprotein E-cadherin which is important in maintaining homophilic cell-cell adhesion in epithelial tissues. E-cadherin interacts with catenin proteins to maintain tissue architecture. Structural defects or loss of expression of E-cadherin have been reported as a common feature in several human cancer types. This study aimed to evaluate the expression of E-cadherin and their correlation with clinical features in microdissected brain tumor samples from 81 patients, divided into 62 astrocytic tumors grades I to IV and 19 medulloblastomas, and from 5 white matter non-neoplasic brain tissue samples. E-cadherin (CDH1) gene expression was analyzed by quantitative real-time polymerase chain reaction. Mann-Whitney, Kruskal-Wallis, Kaplan-Meir, and logrank tests were performed for statistical analyses. We observed a decrease in expression among pathological grades of neuroepithelial tumors. Non-neoplasic brain tissue showed a higher expression level of CDH1 gene than did neuroepithelial tumors. Expression of Ecadherin gene was higher in astrocytic than embryonal tumors (P = 0.0168). Low-grade malignancy astrocytomas (grades I-II) showed higher CDH1 expression than did high-grade malignancy astrocytomas (grades III-IV) and medulloblastomas (P < 0.0001). Non-neoplasic brain tissue showed a higher expression level of CDH1 gene than grade I malignancy astrocytomas, considered as benign tumors (P = 0.0473). These results suggest that a decrease in E-cadherin gene expression level in high-grade neuroepithelial tumors may be a hallmark of malignancy in dedifferentiated tumors and that it may be possibly correlated with their progression and dissemination.

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“…Cell adhesion is a hallmark of prostate cancer cells. E-cadherin, N-cadherin, β -catenin, integrins, focal adhesion kinase, connexins and matrix metalloproteinases all appear to be promising biological markers associated with the early stage metastatic process in prostate cancer [45]. Another module PCDM2 (Figure 3B) is related to receptor binding.…”

Section: Resultsmentioning

confidence: 99%

Detecting disease associated modules and prioritizing active genes based on high throughput data

Qiu

Zhang

et al. 2010

BMC Bioinformatics

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BackgroundThe accumulation of high-throughput data greatly promotes computational investigation of gene function in the context of complex biological systems. However, a biological function is not simply controlled by an individual gene since genes function in a cooperative manner to achieve biological processes. In the study of human diseases, rather than to discover disease related genes, identifying disease associated pathways and modules becomes an essential problem in the field of systems biology.ResultsIn this paper, we propose a novel method to detect disease related gene modules or dysfunctional pathways based on global characteristics of interactome coupled with gene expression data. Specifically, we exploit interacting relationships between genes to define a gene's active score function based on the kernel trick, which can represent nonlinear effects of gene cooperativity. Then, modules or pathways are inferred based on the active scores evaluated by the support vector regression in a global and integrative manner. The efficiency and robustness of the proposed method are comprehensively validated by using both simulated and real data with the comparison to existing methods.ConclusionsBy applying the proposed method to two cancer related problems, i.e. breast cancer and prostate cancer, we successfully identified active modules or dysfunctional pathways related to these two types of cancers with literature confirmed evidences. We show that this network-based method is highly efficient and can be applied to a large-scale problem especially for human disease related modules or pathway extraction. Moreover, this method can also be used for prioritizing genes associated with a specific phenotype or disease.

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

Cited by 34 publications

References 35 publications

Identification of androgen-regulated genes in human prostate

Identification of androgen-regulated genes in human prostate

Differential expression of E-cadherin gene in human neuroepithelial tumors

Detecting disease associated modules and prioritizing active genes based on high throughput data

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