| First Author | Nguyen PM | Year | 2020 |
| Journal | Cell Death Differ | Volume | 27 |
| Issue | 2 | Pages | 742-757 |
| PubMed ID | 31296963 | Mgi Jnum | J:296081 |
| Mgi Id | MGI:6441346 | Doi | 10.1038/s41418-019-0383-9 |
| Citation | Nguyen PM, et al. (2020) Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer. Cell Death Differ 27(2):742-757 |
| abstractText | 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. |
