Understanding the regulation of autophagy in liver cancer

The preservation of cellular homeostasis is fundamental in protecting us against various forms of disease. One process central to the maintenance of homeostasis is macroautophagy (often referred to more simply as autophagy). This processes, which literally means ‘self-eating’, traffics cytoplasmic material to lysosomes for degradation. This results in the removal of damaged proteins and organelles. The constituent parts resulting from this breakdown are either further catabolized to make energy or recycled into biosynthetic pathways. In the context of cancer, autophagy is a major mechanism of tumour suppression as damaged cells are more prone to tumour development. In addition, however, many studies have shown that cells in established tumours are also dependent on autophagy for their survival by mitigating various forms of cellular stress. This therefore raises an apparent paradox where developing tumours must overcome the tumour suppressive effects of autophagy and then reinstate autophagy for the survival of the established tumour. In this regard, we have recently found that an essential autophagy gene may be temporally regulated to explain this collective observations. In this project the student will use molecular cell biology, bioinformatics and genetic techniques to understand the regulation to this gene in cancer progression. The results will also be validated and further explored in models of hepatocellular carcinoma, a cancer type where autophagy is heavily implicated and that is currently undergoing a rapid increase in incidence due, in part, to lifestyle choices that lead to inflammation and damage in the liver.

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