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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.
Highlights
Defects in the single layer of epithelial cells that line the gastrointestinal (GI) tract are implicated in the pathogenesisThese first authors contributed : Paul M
There was no change in the expression of other Bcl-2 family members within the colon of Bcl-g−/− mice, making it unlikely that the function of Bcl-G in adult colonic crypts was masked by compensatory expression of other members of the Bcl-2 protein family (Fig. 1g)
The alternative splice acceptor site that is used to produce BCL-Gs is not conserved across other species, for this reason we utilized mouse Bcl-G, as the closest homolog to understand the biological function of human BCL-GL
Summary
Defects in the single layer of epithelial cells that line the gastrointestinal (GI) tract are implicated in the pathogenesis. Bcl-2, BclXL, Bcl-w, Mcl-1, and A1 form the pro-survival subgroup, and each contain four BH domains (BH1 to BH4). These proteins bind to Bak and Bax, thereby inhibiting their function [5]. HBCL-GS only harbors the BH3 domain, which is recognized as the critical death domain, leading to the suggestion that it is a member of the pro-apoptotic Bcl-2 family subgroup [7]. MBcl-G does not interact with the pro-survival members of the Bcl-2 family through its BH3 domain, suggesting that it is not directly involved in the intrinsic cell-death pathway [7, 9]. The tumor suppressive phenotype associated with Bcl-g is consistent with the observation that BCL-G expression is reduced in late stage human CRC tumors
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