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Conservation over three mammalian genera—the mouse, rat, and human—has been found for a subset of the transcripts whose level differs between the adenoma and normal epithelium of the colon.  Pde4b  is one of the triply conserved transcripts whose level is enhanced both in the colonic adenoma and in the normal colonic epithelium, especially adjacent to adenomas. It encodes the phosphodiesterase PDE4B, specific for cAMP. Loss of PDE4B function in the  Apc   Min/+   mouse leads to a significant increase in the number of colonic adenomas. Similarly,  Pde4b -deficient  Apc   Min/+   mice are hypersensitive to treatment by the inflammatory agent DSS, becoming moribund soon after treatment. These observations imply that the PDE4B function protects against  Apc   Min  -induced adenomagenesis and inflammatory lethality. The paradoxical enhancement of the  Pde4b  transcript in the adenoma versus this inferred protective function of PDE4B can be rationalized by a feedback model in which PDE4B is first activated by early oncogenic stress involving cAMP and then, as reported for frank human colon cancer, inactivated by epigenetic silencing.

plos genetics

The conserved protective cyclic AMP-phosphodiesterase function PDE4B is expressed in the adenoma and adjacent normal colonic epithelium of mammals and silenced in colorectal cancer