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Cellular identity theft leads to cancer metastasis

last modified Jun 07, 2018 02:14 PM

The spread of cancers to distant organs, or metastasis, is responsible for the majority of cancer-related deaths. How cancers develop the capability to spread has remained mostly unclear, however. New research led by Dr. Sakari Vanharanta at the Unit, University of Cambridge, has now identified molecular mechanisms that allow cancer cells to acquire characteristics from other cell types, such as white blood cells, in order to spread and form metastasis.

 Each cell in our body carries the same genes. Yet, due to differences in the ways cells read their DNA, and consequently express their genes, tissues behave differently. Gene expression is orchestrated by tissue-specific networks of gene regulatory elements called transcriptional enhancers, i.e. DNA sequences that control when and where specific genes should be expressed. Enhancers are therefore critical determinants of cellular identity. The new work, published in Cancer Discovery, sheds light on how cancer cells read DNA in unique ways, leading to vastly different behaviours, such as variability in metastatic potential. The work demonstrates how some cancer cells are able co-opt tissue-specific enhancers from unrelated cell types in order to activate genes that support metastatic progression. Through inappropriate enhancer activation cancer cells thus ‘steal’ features from normal cells, consequently facilitating metastatic spread.

 The new observations provide fundamental insight into a long-standing biological and clinical problem of metastasis, and they suggest that therapeutic approaches that would limit the capability of cancer cells to aberrantly activate enhancers could inhibit metastasis in patients.


The study entitled NF-κB–Dependent Lymphoid Enhancer Co-option Promotes Renal Carcinoma Metastasis by Rodrigues et al. has been published in Cancer Discovery on 6 June, 2018.

The article has also been covered as a feature by New Scientist and on the MRC website.