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

2020-02

Nguyen, Paul M

Dagley, Laura F

Preaudet, Adele

Lam, Nga

Giam, Maybelline

Fung, Ka Yee

Aizel, Kaheina

van Duijneveldt, Gemma

Tan, Chin Wee

Hirokawa, Yumiko

Yip, Hon Yan K

Love, Christopher G

Poh, Ashleigh R

Cruz, Akshay D'

Burstroem, Charlotte

Feltham, Rebecca

Abdirahman, Suad M

Meiselbach, Kristy

Low, Ronnie Ren Jie

Palmieri, Michelle

Ernst, Matthias

Webb, Andrew I

Burgess, Tony

Sieber, Oliver M

Bouillet, Philippe

Putoczki, Tracy L

Journal Article

0000-0001-9695-7218

0000-0002-2629-4778

10.1038/s41418-019-0383-9

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.

link

Cell death and differentiation 2020; 27(2): 742-757

Cell death and differentiation