Research Projects

MYC is deregulated in majority of human cancer and it is shown to be critical for the progression and survival of cancer cells. Therefore, an effective strategy to target MYC is one of the attractive cancer treatment avenues. PLK1 is overexpressed in many cancer types and has been shown to be required for MYC overexpressing cells. MYC is known to regulate PLK1 at the transcriptional level but our preliminary result shows that PLK1 and many of the coregulators (Scaffold proteins and activating kinases) were upregulated in MYC overexpressing pancreatic neuroendocrine tumours suggesting that MYC could potentially regulate PLK1 through multiple mechanisms. Therefore, delineating the molecular mechanism of the MYC-PLK1 axis and understanding the indirect regulation of PLK1 through its coregulators is important. Furthermore, considerable efforts were made to understand the role of coregulators for PLK1 function during mitosis but molecular regulators involved in the non-mitotic function of PLK1 is poorly understood. Hence, this proposal aims to address the following open questions. Does MYC regulate PLK1 interactome collectively? Do the known scaffold proteins also play a critical role for PLK1 mediated non-mitotic function? Can we expand the interacting partners of PLK1? Are pancreatic neuroendocrine cells sensitive to PLK1 inhibition?