Loss of Bcl-G, a Bcl-2 family member, augments the development of inflammation-associated colorectal cancer Academic Article uri icon

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.

authors

  • Nguyen, Paul M
  • Dagley, LF
  • Preaudet, A
  • Lam, N
  • Giam, M
  • Fung, KY
  • Aizel, K
  • van Duijneveldt, G
  • Tan, CW
  • Hirokawa, Y
  • Yip, HYK
  • Love, CG
  • Poh, Ashleigh R
  • Cruz, AD
  • Burstroem, C
  • Feltham, Rebecca
  • Abdirahman, SM
  • Meiselbach, K
  • Low, RRJ
  • Palmieri, M
  • Ernst, Matthias
  • Webb, AI
  • Burgess, T
  • Sieber, OM
  • Bouillet, P
  • Putoczki, TL

publication date

  • 2020