Firefly luciferase - the protein that makes fireflies light up - could illuminate a path to accelerated cancer-drug research.
In a study just published in Proceedings of the National Academy of Sciences, Stanford's Sanjiv Gambhir, MD, PhD, and his colleagues sawed the gene encoding for Firefly luciferase in two, then stapled the resulting pieces to the genes for two other proteins whose interaction strongly reflects tumor-cell status.
One of those two proteins was c-Myc, a powerful player in cell growth, proliferation, differentiation and death. Too much c-Myc activity shifts a cell into overdrive, and practically all cancers involve at least some degree of c-Myc hyperactivity. The glass-is-half-full spin on this observation is that drugs that shut down c-Myc (such as atorvastatin, aka Lipitor) are obvious candidates to investigate for treating cancer.
Back to the study: Gambhir and his colleagues were able to get cells containing both bioengineered genes to light up whenever the two resulting "fusion proteins" rubbed up against one another - which happens when, and only when, c-Myc is in an active state. This let the scientists noninvasively image c-Myc activity levels in cultured cells and live animal tissues, just by checking on the light the cells gave off.
The researchers also showed that administering compounds known to inhibit the two proteins' interaction resulted in diminished brightness in the tumor cells - suggesting a quick and efficient way to monitor the effectiveness of experimental drugs that work by targeting c-Myc.
It would really speed things up if anti-cancer drugs' effects on c-Myc activity can be monitored in living tissue. Gambhir's approach, while still in its early days, looks to be a bright idea.
Photo by qmnonic
