Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer
Journal Title
Cell Death and Differentiation
Publication Type
Journal Article in press
Abstract
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.
Publisher
Springer Nature
WEHI Research Division(s)
Personalised Oncology; Advanced Technology And Biology; Inflammation; Structural Biology
PubMed ID
31296963
Open Access at Publisher's Site
https://doi.org/10.1038/s41418-019-0383-9
Rights Notice
Refer to copyright notice on published article.


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