My project consists of investigating the influence of specific Akt isoforms on the pathways involved in the induction of epithelial-mesenchymal transition (EMT). The goal is to determine whether Akt isoforms differentially regulate the expression of members of miR200 family, which are implicated in EMT, and are down-regulated in Tumor Initiating Cells (TICs). We will also fully characterize the perturbed pathways in claudin-low subtype versus other subtypes of breast cancer, as this particular subtype is highly enriched in TICs. TICs are thought to be responsible for tumor resistance to drug treatment, as well as for the cancer relapse. It is therefore crucial to understand what molecular pathways govern the proliferation and survival of TICs, in order to design better therapies for patients with breast cancer.
- Joined Lab: May 2010
- Position: Graduate Student - Molecular Cell Biology Program
- Degree: B.S., University of Belgrade