A loss-of-function RNA interference screen for molecular targets in cancer

Vu N. Ngo, R. Eric Davis, Laurence Lamy, Xin Yu, Hong Zhao, Georg Lenz, Lloyd T. Lam, Sandeep Dave, Liming Yang, John Powell and Louis M. Staudt ()
Additional contact information
Vu N. Ngo: National Cancer Institute
R. Eric Davis: National Cancer Institute
Laurence Lamy: National Cancer Institute
Xin Yu: National Cancer Institute
Hong Zhao: National Cancer Institute
Georg Lenz: National Cancer Institute
Lloyd T. Lam: National Cancer Institute
Sandeep Dave: National Cancer Institute
Liming Yang: CIT, National Institutes of Health
John Powell: CIT, National Institutes of Health
Louis M. Staudt: National Cancer Institute

Nature, 2006, vol. 441, issue 7089, 106-110

Abstract: Making the most of RNAi Two papers this week highlight the impact of RNAi (RNA interference) in clinical medicine. Ngo et al. have developed a novel ‘Achilles heel' screen to identify genes that, if silenced, cause cancer cells to stop dividing. The novelty lies in a successful ‘negative’ screen that can reveal potential therapeutic targets that do not necessarily contain mutations or other alterations. Use of the screen on 2,500 genes in B-cell lymphoma cells identified three genes that were essential for cancer cell survival and growth of one particular B-cell lymphoma subtype. In particular the protein CARD11 looks a prime target. Zimmermann et al. report a significant step towards harnessing RNAi as a new class of drug treatment. They used systemic administration of small interfering RNA (siRNA) to silence a disease-causing gene in a non-human primate: it had previously been demonstrated in mice. Specifically, siRNA targeted against the gene for apolipoprotein B (ApoB) in cynomolgus monkeys successfully reduced in ApoB protein, serum cholesterol and low-density lipoprotein levels. This has implications for diseases associated with high cholesterol levels, such as coronary heart disease, and more broadly demonstrates that potential therapies may be developed against historically ‘non-druggable’ targets.

Date: 2006
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DOI: 10.1038/nature04687

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