Some cancers could have an epigenetic origin

Some cancers could have an epigenetic origin
Some cancers could have an epigenetic origin

The origin and development of cancers are due to the interplay of genetic, epigenetic and environmental factors. The dominant approach gives preponderance to genetic mutations, considered to be the main causal factor. However, the role of epigenetic factors appears increasingly important. A decisive step has been taken by an international team including researchers from the University of Montpellier and the CNRS (National Center for Scientific Research). Published in the journal Naturehis work indeed provides strong arguments for the possibility that epigenetic factors alone can induce and maintain cancer.

She was interested in the Polycomb protein complex (PcG – Polycomb Group), which exists in many organisms, from the Drosophila fly to humans. This complex has the property of modifying chromatin in order to suppress the expression of certain genes, in particular those of embryonic development. Alterations in its functioning lead to developmental abnormalities and cancers.

The researchers caused a decrease in the amount of PcG in the cell nuclei of fruit flies. This led to the activation of genes coding for molecules of the JAK-STAT intranuclear signaling pathway, involved in transcription, and the appearance of cancer processes. However, the restitution of normal quantities of PcG does not result in the suppression of the activity of the genes coding for the JAK-STAT pathway. This means that the transient decrease in PcG led to a constant phenomenon by triggering a self-sustaining process, the expression of genes encoding the JAK-STAT pathway, with the consequence of the appearance and maintenance of cancers.

Generally speaking, this result allows us to postulate that an epigenetic process is capable of generating and fueling a cancerous process on its own. This hypothesis is supported by the fact that PcG is present in a wide variety of living beings and that it is therefore possible to assume that the extrapolation of the results of this work beyond Drosophila alone is legitimate. Furthermore, for the authors, their work is consistent with several previous observations. For example, it has been shown in several cohorts of patients with multiple myeloma that decreased expression of genes encoding PcG is associated with poor prognosis. The authors suggest that future work further examine the role of epigenetic disruptions in this and other pathologies.

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