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.
Keywords