| Discovery
of role of Id1 gene in angiogenesis may lead to new therapeutic targets
for cancers with active Id1 expression The discovery that the gene Id1, which is highly expressed in many cancers, controls a molecular switch for angiogenesis may lead to new targets for treatment, according to an article in the December 17th issue of Cancer Cell. The American team found that the Id1 gene can control angiogenesis by turning off production of a natural suppressor, the protein thrombospondin-1. "We found activation of the Id1 gene, which is highly expressed in melanoma, breast, head and neck, brain, cervical, prostate, pancreatic, and testicular cancers, results in decreased expression of thrombospondin-1 and increased tumor blood vessel formation," said Rhoda M. Alani, M.D., director of the study and the article’s senior author. The researchers’ initial finding was that levels of thrombospondin-1 were 3-fold to 5-fold greater in mice without Id1 gene function than in mice with normal Id1 function. To confirm the correlation, the research team monitored blood vessel growth in mice with normal and nonfunctional Id1 genes. Control mice with normal Id1 gene function showed well-developed blood vessels. Mice with a nonfunctional Id1 gene showed little blood vessel growth and notable thrombospondin-1 activity. When the anti-thrombospondin chemical was given to these mice, angiogenesis resumed. Efforts to find a way to use thrombospondin-1
as an anti-cancer agent are under way in animal studies. "Because
thrombospondin-1 occurs naturally throughout the body, it can't
be used as a drug," said Roberto Pili, M.D., a coauthor of
the study. "But it could potentially be paired with another
molecule and programmed to be released only in tumors." |