Research ArticleCancer

Targeting of AML1-ETO in t(8;21) Leukemia by Oridonin Generates a Tumor Suppressor–Like Protein

See allHide authors and affiliations

Science Translational Medicine  28 Mar 2012:
Vol. 4, Issue 127, pp. 127ra38
DOI: 10.1126/scitranslmed.3003562

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Herbal Fusion

High-tech gadgets and designer medicines increasingly drive medical treatment. But newer isn’t always better, and there has been a revitalized push for “natural” and “herbal” remedies. Although evidence supporting some of these therapies is shaky at best, researchers have found solid scientific bases for others—isolating active compounds with well-established biological function. One such compound is oridonin. Originally identified as a component of the herb Isodon rubescens, oridonin selectively kills leukemic cells that express a particular oncoprotein. Now, Zhen et al. show us exactly how compound works.

Acute myeloid leukemia (AML) is a cancer of myeloid cells in the blood and bone marrow. The AML1-ETO fusion protein—an oncoprotein that results from a chromosomal translocation found in a subset of AML patients—is cleaved as a result of oridonin exposure. In the current study, the authors demonstrated that oridonin has two functions within AML1-ETO+ AML cells. The drug bound and blocked components of the oxidative damage prevention system, glutathione and thioredoxin/thioredoxin reductase, which resulted in increased amounts of reactive oxygen species and activated caspase-3. Oridonin also specifically bound to AML1-ETO, causing it to be cleaved into a truncated version that acted as a tumor suppressor in the AML cells. These data show how a simple herb can contribute a lead compound for personalized therapy in AML1-ETO+ AML patients.

View Full Text

Stay Connected to Science Translational Medicine