Cancer-linked protein needs a partner to activate silent DNA, fruit fly experiments reveal
In Ewing sarcoma, an abnormal protein formed by the fusion of two genes can activate repetitive DNA regions that normally remain silenced and turn them into gene regulatory elements. This mechanism contributes significantly to the development of this tumor and is one of its best-studied molecular hallmarks.
New research published in G3: Genes, Genomes, Genetics reveals that a protein linked to cancer, called ETV4, can activate genetic regions in fruit flies that are typically silent. Normally, these regions, known as GGAA microsatellites, remain inactive. However, when ETV4 works together with a protein called Cabeza—a counterpart to the human protein FET—the DNA regions become active.
This discovery provides insight into how cancer-linked proteins can manipulate genetic activity, potentially shedding light on cancer development beyond Ewing sarcoma. The findings were made possible by studying Drosophila melanogaster, a fruit fly model, which allowed scientists to observe the effects of protein partnerships across a wide evolutionary distance.
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