Cancers become aggressive when some cells fall into a stereotyped genetic program reminiscent of the “epithelial-mesenchymal transition” (EMT). The mesenchymal state is inherited from ancestral unicellular evolutionary stages. In metazoans, it acquired functions in development and wound healing. Tumoral EMT involves several hundred genes in a coordinated manner, which collectively generate the metastatic phenotype (cellular individualization, exacerbated proliferation, migration and tissue infiltration, switches in biosynthetic and energetic metabolisms etc). The EMT is a remarkable example of global gene expression switch associated to genome-wide epigenetic changes. We are studying the transcriptional mechanisms underlying EMT involved in breast cancer aggravation, and their sensitivity to environmental conditions.

Our research is divided into several projects:

Transcriptional gene expression regulation and alterations in cancer
Basic transcriptional regulation mechanisms. Mechanisms specifically involved in the epithelial-mesenchymal transition, particularly in breast cancer context involving estrogen receptor.

Physical and chemical environmental agents impact on gene expression

Figure: Typical cell phenotype changes associated to EMT