Epithelial Mesenchymal Transition (EMT) provide tumour cells with the ability to migrate and invade secondary sites while Mesenchymal Epithelial Transition (MET), may then allow establishment and proliferation of the malignant tumour cells. The term, Epithelial Mesenchymal Plasticity (EMP), encompasses the interconversions between epithelial and mesenchymal states. We have been able to demonstrate marked similarities between the aggressive basal breast cancer cell lines and cells that have undergone an EMT. Epithelial cell adhesion molecule (EpCAM) is widely used clinically to isolate circulating (CTC) and disseminated (DTC) tumour cells from patient samples. EpCAM is significantly downregulated in basal breast cancer cell lines and studies show EpCAM downregulation following an EMT.
The basal like EpCAM +ve PMC42LA cells have been transduced with a boutique shRNA library targeting the genes responsible for maintenance of cell polarity and markers of Breast Cancer Stem Cells, EMP and metastasis. EpCAM low cells isolated from this transduced population display a mesenchymal morphology while EpCAM high cells are more proliferative. Using FACS, these populations have been sorted and currently awaiting next generation sequencing for identification of hairpins enriched within these phenotypes. Further studies would incorporate the utilisation of individual hairpins and subsequent functional studies in vitro and in vivo to identify to role of these genes in cancer biology.