RAC GTPase signalling in lung cancer

Hosted by the School of Cellular and Molecular Medicine

Host: Anne Ridley

My laboratory has been focusing on cell migration and invasion— processes required for metastasis of cancer cells— and their control by Rho-like molecules, small G proteins that constitute a subfamily of the RAS oncoprotein superfamily. We have revealed that signalling by the small GTPase RAC1 not only promotes cell migration (as widely reported in the literature) but can also inhibit migration dependent on context. We have also uncovered multiple determinants of this dual function of RAC1 and several mechanisms by which RAC1 activation either promotes or inhibits migration. We have thereby revealed ways to selectively inhibit the pro-tumorigenic functions of this GTPase, which is a critical oncogenic mediator. More recently we have been focusing on lung cancer, the leading cause of cancer deaths worldwide. We have been focusing on KRAS-mutant non-small cell lung cancer as well as small cell lung cancer and I will describe recent data from my laboratory evaluating components of RAC signalling as molecular targets in these two lung cancer types. 

Institutional profile