Pathway Discovery holds Potential for Targeted Treatments

Having discovered that the journey or molecular pathway of an identified protein is essential for brain development, researchers at Queen’s University Belfast have also determined that any alteration to its pathway could result in the spread of cancer throughout the body.

Epithelial to Mesenchymal Transition (EMT) is a particular molecular pathway that enables cell migration; it is vital for early development processes including brain development as well as for wound healing later in life but is also used by cancer cells for metastasis. With the research team having identified a particular protein, ZNF827, as a critical regulator of EMT, the study(1) shows the importance of the molecular pathway of proteins for migration of newborn neurons, but also its potential as a route for cancer to metastasize to different organs. 

Lead Author, Dr Vijay Tiwari from the Wellcome-Wolfson Institute for Experimental Medicine at Queen’s University, said: “Our study not only sheds light on the development of one of the most important organs in our body – the brain – but it also shows how the same protein that is key for brain development can also be the cause or target for the spread of cancer in the body, a real Jekyll and Hyde protein. 

“The process for migrating newborn neurons to proper places during brain development is the same process exploited by tumour cells to gain migration potential, causing the movement of cancer throughout the body, or cancer metastasis. 

“By identifying key regulators of these pathways, we open new opportunities for a therapeutic intervention against cancer and a better understanding of neurodevelopmental disorders involving defects in brain development.” 

The international team includes researchers from Queen’s University Belfast, Salk Institute for Biological Studies, Altos Labs, University of Montpellier, Karolinska Institutet, University Medical Center of the Johannes Gutenberg University Mainz and Translational Oncology at the University Medical Center of the Johannes Gutenberg University Mainz gGmbH (TRON gGmbH). 

This study was supported by the Deutsche Forschungsgemeinschaft, Wilhelm Sander Stiftung and Innovation to Commercialisation of University Research programme. 

(1)  Published in Nature Cell Biology

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