Differential expression of boc, spock2, and gjd3 is associated with brain metastasis of er-negative breast cancers

Rute M.S.M. Pedrosa, Leonoor V. Wismans, Renata Sinke, Marcel van der Weiden, Casper H.J. van Eijck, Johan M. Kros, Dana A.M. Mustafa*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

4 Citations (Scopus)
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Background: Brain metastasis is considered one of the major causes of mortality in breast cancer patients. To invade the brain, tumor cells need to pass the blood-brain barrier by mechanisms that are partially understood. In primary ER-negative breast cancers that developed brain metastases, we found that some of the differentially expressed genes play roles in the T cell response. The present study aimed to identify genes involved in the formation of brain metastasis independently from the T cell response. Method: Previously profiled primary breast cancer samples were reanalyzed. Genes that were found to be differentially expressed were confirmed by RT-PCR and by immunohistochemistry using an independent cohort of samples. Results: BOC, SPOCK2, and GJD3 were overexpressed in the primary breast tumors that developed brain metastasis. BOC expression was successfully validated at the protein level. SPOCK2 was validated at both mRNA and protein levels. SPOCK2 and GJD3 mRNA overexpression were also found to be associated with cerebral metastasis in an external online database consisting of 204 primary breast cancers. Conclusion: The overexpression of BOC, SPOCK2, and GJD3 is associated with the invasion of breast cancer into the brain. Further studies to determine their specific function and potential value as brain metastasis biomarkers are required.

Original languageEnglish
Article number2982
Issue number12
Publication statusPublished - 15 Jun 2021

Bibliographical note

Funding Information:
This work was partially funded by the Dutch Cancer Society (KWF), grant number EMCR 2009-4553, by the Department of Pathology, Erasmus MC, and by the OAK Foundation.

Publisher Copyright:
© 2021 by the authors. Licensee MDPI, Basel, Switzerland.


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