IMR Press / FBE / Volume 3 / Issue 2 / DOI: 10.2741/E274

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Molecular alterations of E-cadherin and beta-catenin in brain metastases
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1 Laboratory of Neuro-oncology, Croatian Institute for Brain Research, School of Medicine University of Zagreb, Salata 12, HR10000 Zagreb, Croatia
2 Department of Biology, School of Medicine, University of Zagreb, Salata 3, HR-10000 Zagreb, Croatia
3 Clinical Institute of Laboratory Diagnosis, Clinical Hospital Centre Zagreb, Kispaticeva 12, 10 000 Zagreb, Croatia
4 Department of Neurosurgery, University Hospital, Sisters of Charity, Vinogradska 29, 10000 Zagreb, Croatia
5 Ljudevit Jurak Department of Pathology, University Hospital, Sisters of Charity, Vinogradska 29, 10000 Zagreb, Croatia
Front. Biosci. (Elite Ed) 2011, 3(2), 616–624; https://doi.org/10.2741/E274
Published: 1 January 2011
Abstract

The molecular mechanisms and candidate genes involved in metastasis to the brain need elucidation. In the present study brain metastases were analyzed regarding changes of E-cadherin (CDH1) and beta-catenin (CTNNB1). Loss of heterozygosity (LOH) of the CDH1 gene was detected in 42.2% of samples. The highest frequency of LOHs was observed in metastases from primary sites of lung adenocarcinoma and small cell lung cancer. Metastases from breast and colon demonstrated changes in 55.6% and 50% of cases. Downregulation of E-cadherin protein was observed in 83% of samples. Only 21.1% of samples with E-cadherin LOH had beta-catenin located in the nucleus. Image analysis showed that the quantities of E-cadherin and beta-catenin were significantly positively correlated (P = 0.008). Changes of E-cadherin were frequent in brain metastases that we investigated. Lack of mutations of beta-catenin, the fact that it was not frequently found in the nucleus and the positive correlation between the two proteins may suggest that the break-up of adherens junctions, and not the activation of wnt signaling, is responsible for metastasis formation.

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