Rockefeller research scientists have found a new way to halt the proliferation of cancer cells, using protein-inhibiting agents called IAP’s (inhibitor of apoptosis protein). The findings are considered a break-through development toward improving cancer outcomes, and may lead to a new class of cancer therapy and prevention drugs. Self-destruction of cancerous cells can occur normally, and the process of amplifying the process in lab mice has yielded success for the research team. The study is the first to show exactly how IAP’s regulate cell death.
Hermann Steller, Strang Professor and head of the Laboratory of Apoptosis and Cancer Biology says, “We now can study how IAPs contribute to the development of cancer in a living animal and develop drugs to prevent or thwart the disease.” The role of IAP’s in preventing programmed cell death has been unclear. Dr. Steller explains, “Cancer cells thrive by disabling the molecular machinery that tells sick cells to die. By removing the RING, we wanted to see whether we would trick the machinery to turn back on. And that’s what happened.
According to the study, mice who were predisposed to cancer, without the IAP ring finger domain “lived twice as long as those with it.” The researchers specifically found that IAP’s that bind to enzymes called capsases, and in turn regulate cell death, are influenced by the RING. The body tries to preserve cells, as increasing numbers of molecular tags are transferred to capsases by the RING. When the RING is removed, and the signals become weaker; the tags are fewer.
There is certainly more to come, as researchers try to find exactly which IAP genes promote cancer. Dr. Steller says, “We need to use genetics to sort out which individual IAPs contribute to tumors and which IAPS we need to target in order to cure cancer. This was a very big step in understanding what role IAPs play in cancer, but it isn’t the last.”
Source: GENES & DEVELOPMENT 22:2256-2266, 2008
©2008 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/Abstract