Gigin Lin1, Dow-Mu Koh1, Simon P. Robinson1, Paul Clarke2, Martin O. Leach1, Yuen-Li Chung1
1Cancer Research UK and EPSRC Cancer Imaging Centre, Institute of cancer research and Royal Marsden Hospital, Sutton, Surrey, United Kingdom; 2Cancer Research UK Centre for Cancer Therapeutics, Institute of cancer research and Royal Marsden Hospital, Sutton, Surrey, United Kingdom
Bax, a Bcl-2 family protein, plays a central role in regulating apoptosis pathways thus being a major determinant of tumour cells fate in response to cancer therapy. 4% of human colorectal carcinoma Hct116 cells are Bax-deficient and are known to be resistant to chemotherapy and TRAIL-induced apoptosis. However, there is little information available on the metabolic effects of Bax-deficiency in colorectal carcinoma cells. We designed a 1H NMR based metabolomics study of isogenic wild type (WT) and Bax-deficient (KO) colorectal carcinoma cells, to examine the metabolic effects of Bax-deficiency in cancer cells. Many metabolic adaptations, including glycolysis, glutaminolysis, serine/purine synthesis and metabolism were found in Bax KO cells when compared with WT cells. This study indicates the functional diversity of Bax-deficiency on colorectal carcinoma Hct116 cells.