Anticancer Sulfonamides Target Splicing By Inducing Rbm39 Degradation Via Recruitment To Dcaf15
SCIENCE(2017)
摘要
Typically, cancer drugs that help only a small number of patients in clinical trials are not pursued. This might change in a future world of precision medicine, where biomarkers will match specific drugs to the patients most likely to respond. Han et al. identified the mechanism of action of a cancer drug called indisulam, a sulfonamide tested previously in patients with solid tumors. Indisulam and related sulfonamides killed cells by disrupting precursor mRNA splicing. The drugs targeted a specific RNA splicing factor for degradation by “gluing” it to the CUL4-DCAF15 ubiquitin ligase. Experiments with cancer cell lines suggest that future clinical trials of these drugs should focus on leukemias and lymphomas with high DCAF15 expression levels.Science , this issue p. [eaal3755][1] [1]: /lookup/doi/10.1126/science.aal3755
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关键词
rbm39 degradation
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