Defects in both apoptosis and autophagy have been linked to cancer development. Members of the Bcl-2 family of proteins are essential regulators of apoptosis, a physiological cell death process. Recently, Bcl-2 family proteins have also been implicated in autophagy, a mechanism that ensures the recycling of cellular organelles. Bcl-G is a new and poorly studied BH3-only member of the Bcl-2 family of proteins whose expression is under the control of the tumour suppressor p53. While Bcl-G has been linked to breast cancer, its function during tumourigenesis is not clear. Our previous results suggest that Bcl-G has a limited role in apoptosis, but may have a role in intracellular vesicular trafficking through its interaction with Trappc6b (1,2). In order to study the physiological function of Bcl-G we generated a knockout mouse, which has increased susceptibility to models inflammatory bowel disease. We further investigated the role of Bcl-G in a colitis-associated colon cancer model, and show that loss of Bcl-G significantly increased tumor burden. We are currently characterizing the function of Bcl-G at a molecular level, in order to understand its role in inflammatory bowel disease and colon cancer.
1) Giam M, et al. Cell Death Dis. 2012. p. e378
2) Miled C, et al. Cancer Res. 2005. p. 5096-104