Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/21483
Title: Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer.
Austin Authors: 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
Affiliation: Research Division, Peter MacCallum Cancer Centre, 305 Grattan St, Melbourne, Australia
Now located at Monash Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria, 3800, Australia
The Department of Medical Biology, The University of Melbourne, Melbourne, Victoria, 3050, Australia
Department of Surgery, The University of Melbourne, Melbourne, Victoria, 3052, Australia
Department of Biochemistry & Molecular Biology, Monash University, Clayton, Victoria, 3800, Australia
Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia
School of Cancer Medicine, La Trobe University, Heidelberg, Victoria, 3084, Australia
The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, 3052, Australia
Issue Date: Feb-2020
metadata.dc.date: 2019-07-11
Publication information: Cell death and differentiation 2020; 27(2): 742-757
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.
URI: http://ahro.austin.org.au/austinjspui/handle/1/21483
DOI: 10.1038/s41418-019-0383-9
ORCID: 0000-0001-9695-7218
0000-0002-2629-4778
PubMed URL: 31296963
Type: Journal Article
Appears in Collections:Journal articles

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