Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer.
Cell Death Differ
; 27(2): 742-757, 2020 02.
Article
de En
| MEDLINE
| ID: mdl-31296963
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.
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Tumeurs colorectales
/
Protéines proto-oncogènes c-bcl-2
/
Inflammation
Type d'étude:
Risk_factors_studies
Limites:
Animals
/
Humans
Langue:
En
Journal:
Cell Death Differ
Année:
2020
Type de document:
Article
Pays d'affiliation:
Australie