APC usually halts cell growth in adults, but defects lead to enhanced cell signaling, which seems to explain its function in colon cancer, according to Science paper.

Dartmouth Medical School (DMS) geneticists report that the gene adenomatous polyposis coli (APC), which normally prevents excessive cell growth, can also accelerate cell signaling. This discovery has led them to a hypothesis of APC’s role in triggering the development of most colorectal cancers.

APC is part of a vital signaling pathway that coordinates cell growth in all animals. During embryonic development, this pathway causes cells to grow and differentiate to become the kind of cells they should be. In many adult cells, however, APC puts the necessary brakes on the pathway to stop cell growth.

When scientists remove or reduce APC in fruit flies, they see flies with no wings, peculiar abdomens, and many other oddities. APC defects found in colonic polyps, however, have an unusual feature. In the polyps, only half the APC protein is lost, while the other half remains, according to the researchers. The research team found that part of the APC protein is involved in increasing the activation of the signaling pathway. They believe this explains the role of the truncated protein in colon cancer. 

Since the pathway is evolutionarly conserved, the investigators believe that APC may also have an activating role in vertebrates with relevance to development and cancer.

This study is reported in the January 18 issue of Science.

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