How does Rme-6 contribute to chemoresistance in triple negative breast cancer?

Triple negative breast cancer (TNBC) is a particularly aggressive form of cancer with poor long-term prognosis. Lacking hormone receptors, TNBC cells often have overexpression and/or mutation of a cell surface protein, epidermal growth factor receptor (EGFR), which, if it is not properly regulated, causes uncontrolled proliferation. There has been some success in the development of chemotherapies for TBNC, especially inhibitors that interfere with the receptor tyrosine kinase activity of EGFR. However, TNBC often becomes resistant to these drugs, leading to recurrence of the disease and subsequent metastasis. We have identified a protein called Rme-6/GAPVD1 which acts as a scaffold, recruiting other molecules important for EGFR proliferative signalling. Importantly, loss of Rme-6 sensitises TNBC cells to chemotherapy agents which suggests that it has good potential as a novel therapeutic target, which could be used in combination with conventional therapies to overcome resistance. We are currently exploring how Rme-6 contributes to chemoresistance by investigating which proteins Rme-6 interacts with to regulate EGFR signalling. The student will use a variety of molecular cell biological approaches including siRNA knockdown, cell culture, immunofluorescence microscopy and proliferation assays to explore the mechanisms by which Rme-6 and its binding partners contribute to chemoresistance. Students will need to find their own accommodation and be expected to present their findings orally at a research day in York on 08th September 2026.