A Washington University research team headed by Shrikant Anant, PhD, is mighty excited about their new discovery that was reported in the journal, Molecular Cell. They have found a "master switch" - a protein named CUBGP2(cytidine-uridine-guanosine binding protein) - that makes cancer cells self-destruct. The findings that were published apply only to cancer cells grown in a test tube. Human studies aren't yet on the drawing board. However, lead researcher Anant said that the protein works across the board for many cancers and that it might become a great tool for cancer therapy.
CUBGP2 has multiple effects but there is one very important effect that stands out from the rest. All normal cells are full of CUBGP2 and when their time comes to die, this protein helps them do so by activating their built-in self-destruct program. But, when these cells start becoming cancerous, they somehow lose CUBGP2 and this leads to build up of large amounts of an enzyme known as Cox-2. Cox-2 is the major culprit in arthritis and headache. Aspirin-like drugs and newer drugs such as Celebrex and Vioxx, known as Cox-2-selective inhibitors, block the action of this enzyme. Cox-2, when over-expressed by precancer cells, helps them grow the new blood vessels they need to become tumors.
Aspirins and the new Cox-2 inhibitors help slow cancer growth, but they have a limited effect. However, when Anant's team put CUGBP2 into cancer cells, they found that more than 70% of them died and the protein also shut off the Cox-2 gene. Anant's colleague Brian K. Dieckgraefe (pronounced de-GRAF) said that this might be an important therapeutic advance and might lead to a considerable amount of new research into a pathway that may have dramatic anticancer effects.