The DCC gene product induces apoptosis by a mechanism requiring receptor proteolysis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1998-10

AUTHORS

Patrick Mehlen, Shahrooz Rabizadeh, Scott J. Snipas, Nuria Assa-Munt, Guy S. Salvesen, Dale E. Bredesen

ABSTRACT

The development of colonic carcinoma is associated with the mutation of a specific set of genes. One of these, DCC (deleted in colorectal cancer), is a candidate tumour-suppressor gene, and encodes a receptor for netrin-1, a molecule involved in axon guidance. Loss of DCC expression in tumours is not restricted to colon carcinoma, and, although there is no increase in the frequency of tumour formation in DCC hemizygous mice, reestablishment of DCC expression suppresses tumorigenicity. However, the mechanism of action of DCC is unknown. Here we show that DCC induces apoptosis in the absence of ligand binding, but blocks apoptosis when engaged by netrin-1. Furthermore, DCC is a caspase substrate, and mutation of the site at which caspase-3 cleaves DCC suppresses the pro-apoptotic effect of DCC completely. These results indicate that DCC may function as a tumour-suppressor protein by inducing apoptosis in settings in which ligand is unavailable (for example, during metastasis or tumour growth beyond local blood supply) through functional caspase cascades by a mechanism that requires cleavage of DCC at Asp 1,290. More... »

PAGES

801-804

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/27441

DOI

http://dx.doi.org/10.1038/27441

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1038963763

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9796814


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