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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; 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
2019-07-11
Cell Death and Differentiation
Journal Article in press
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.
Springer Nature
Personalised Oncology; Advanced Technology and Biology; Inflammation; Structural Biology
10.1038/s41418-019-0383-9
31296963
Refer to copyright notice on published article.

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Creation Date 2019-07-17 01:31:57 Last Modified 2019-07-17 02:04:42