We study the emerging roles of noncoding RNAs as key regulators of gene expression in physiological cellular programmes and at the onset or during progression of human diseases, with a major focus on tumorigenesis and neurodevelopmental diseases. The research carried out by our group combines biochemical, cellular and global genomic approaches to dissect mechanisms of gene expression regulation with the participation of ncRNAs, with the ultimate aim of revealing molecules of therapeutic/biomarker interest for clinical translation.
The lab focuses on a variety of RNA and RNA-binding protein functions in the context of changing cellular conditions. Our interest concentrates on the noncoding transcriptome, with the main aim of separating the wheat from the chaff to reveal true biologically relevant molecules and to understand how they are connected to broader gene regulatory networks.
Cancer research has led the way in the study of noncoding RNAs, but the abundance and key roles of the noncoding transcriptome in the human brain are being increasingly recognized. Importantly, common dysregulated mechanisms in different pathological contexts and with the involvement of ncRNAs, are emerging.
Our research aims to gain a better understanding of the biological relevance of ncRNAs for an informed use in therapeutic strategies. Recently, our group’s research has taken advantage of state-of-the-art global transcriptomic approaches to identify ncRNA candidates that act as master regulators of oncofoetal genes, thereby revealing their validity as biomarkers in human cancer.
In addition to our work related to cancer, the group has been developing new experimental tools for research into Rett syndrome, a neurodevelopmental disorder usually caused by loss-of-function mutations in the epigenetic regulator MeCP2.
Through our research, we hope to answer the following questions:
What is the precise contribution of the non-coding transcriptome to tumour biology?
How can we use RNA tools to improve treatment or diagnosis of human disease?
How can we better model neurodevelopmental diseases such as Rett syndrome to understand key initial changes in gene expression programmes?