About this Webinar:
Breast cancer is the most common and deadliest cancer in women worldwide. While early-stage is curable in 75% of patients, advanced metastatic breast cancer remains largely incurable with current therapies. Breast cancer is an heterogenous disease categorized into three main subtypes based on the expression of key markers orientating specific treatment strategies for each subtype. The complexity of breast carcinogenesis is often associated with epigenetic modification regulating signaling pathways involved in breast tumor initiation, progression and relapse to treatments. In this context, my team is interested in the role of Protein Arginine Methyl Transferases (PRMTs) in the signaling of steroid receptors in different subtypes of breast cancer.
We have shown that PRMT1, by methylating the estrogen receptor ERα, regulates the estrogen non genomic signaling, participating in the resistance to endocrine therapy. More recently, we found that in triple negative breast cancer, PRMT5 forms a complex with the glucocorticoid receptor (GR), regulating the transcription of genes involved in motility, thereby promoting glucocorticoid-induced cell migration. On the contrary, in ERα+ tumors, although cytoplasmic PRMT5 possesses oncogenic properties, nuclear PRMT5 is a predictive biomarker of response to anti-estrogens. Using innovative proteomic approaches, we are currently investigating how PRMT5 nuclear shuttling is regulated to favor its nuclear localization and maximize the response to anti-estrogens therapy.
