Important role of p53 in regulating LM expression in IBD and colitis-associated cancer.

<p>We propose the following scenario where inflammation triggers nuclear accumulation of p53 that transactivates expression of LMα1 and its deposition to the BM concomitantly to that of LMα5. Overexpression of LMα5 in response to inflammation is a p53 independent mechanism. In a chronically inflamed microenvironment highly expressed LMα1 and LMα5 may provide physical barrier function resulting in attenuated inflammation as demonstrated in transgenic mice. Yet, high LMα1 and LMα5 in a carcinogenic setting subsequent to chronic colitis may contribute to a pro-tumorigenic microenvironment.