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Manipulating the tumour-suppressor protein Rb in lung cancer reveals possible drug targets

Tumours often become resistant to treatment, but how this occurs is poorly understood. An analysis of how the protein Rb affects tumour growth and the response to therapy might cast light on the problem.
  1. Seth M. Rubin

    1. Seth M. Rubin is in the Department of Chemistry and Biochemistry, University of California, Santa Cruz, Santa Cruz, California 95064, USA.

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  2. Julien Sage

    1. Julien Sage is in the Departments of Pediatrics and of Genetics, Stanford University, Stanford, California 94305, USA.

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The development of cancer invariably involves cellular proteins that have unwanted effects or that become inactive. Therapeutically targeting proteins that are more active than normal is conceptually straightforward — a drug needs to be found that, like a wrench thrown into a machine, halts the malicious activity. By contrast, remedying the loss of a type of protein called a tumour suppressor, which normally opposes cancer growth, presents a conundrum. How can a protein be targeted by drugs if it is no longer present? One way of getting around this problem and finding new drug targets is to identify other effects, such as molecular changes, that occur when a tumour suppressor is lost or does not function. Writing in Nature, Walter et al.1 report their analysis of the role of the tumour-suppressor protein retinoblastoma (Rb), using an experimental system that allowed them to engineer the loss and reactivation of this protein in lung cancer in mice.

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Nature 569, 343-344 (2019)

doi: https://doi.org/10.1038/d41586-019-01319-y

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