Biochemistry and Pharmacology - Research Publications

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Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer

Nguyen, PM ; Dagley, LF ; Preaudet, A ; Lam, N ; Giam, M ; Fung, KY ; Aizel, K ; van Duijneveldt, G ; Tan, CW ; Hirokawa, Y ; Yip, HYK ; Love, CG ; Poh, AR ; D' Cruz, A ; Burstroem, C ; Feltham, R ; Abdirahman, SM ; Meiselbach, K ; Low, RRJ ; Palmieri, M ; Ernst, M ; Webb, AI ; Burgess, T ; Sieber, OM ; Bouillet, P ; Putoczki, TL (NATURE PUBLISHING GROUP, 2020-02)

Gastrointestinal epithelial cells provide a selective barrier that segregates the host immune system from luminal microorganisms, thereby contributing directly to the regulation of homeostasis. We have shown that from early embryonic development Bcl-G, a Bcl-2 protein family member with unknown function, was highly expressed in gastrointestinal epithelial cells. While Bcl-G was dispensable for normal growth and development in mice, the loss of Bcl-G resulted in accelerated progression of colitis-associated cancer. A label-free quantitative proteomics approach revealed that Bcl-G may contribute to the stability of a mucin network, which when disrupted, is linked to colon tumorigenesis. Consistent with this, we observed a significant reduction in Bcl-G expression in human colorectal tumors. Our study identifies an unappreciated role for Bcl-G in colon cancer.