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Small molecule inhibition of ERK dimerization prevents tumorigenesis by RAS-ERK pathway oncogenes

AuthorsHerrero, Ana; Pinto, Adán; Colón-Bolea, Paula; Casar, Berta ; Agudo-Ibáñez, Lorena; Vidal, Rebeca ; Valdizán, Elsa M. ; Rivas, Germán ; Pazos, Ángel ; Crespo, Piero
Issue Date2015
PublisherCell Press
CitationCancer Cell 28(2): 170-182 (2015)
AbstractNearly 50% of human malignancies exhibit unregulated RAS-ERK signaling; inhibiting it is a valid strategy for antineoplastic intervention. Upon activation, ERK dimerize, which is essential for ERK extranuclear, but not for nuclear, signaling. Here, we describe a small molecule inhibitor for ERK dimerization that, without affecting ERK phosphorylation, forestalls tumorigenesis driven by RAS-ERK pathway oncogenes. This compound is unaffected by resistance mechanisms that hamper classical RAS-ERK pathway inhibitors. Thus, ERK dimerization inhibitors provide the proof of principle for two understudied concepts in cancer therapy: (1) the blockade of sub-localization-specific sub-signals, rather than total signals, as a means of impeding oncogenic RAS-ERK signaling and (2) targeting regulatory protein-protein interactions, rather than catalytic activities, as an approach for producing effective antitumor agents.
Descriptionet al.
Identifiersdoi: 10.1016/j.ccell.2015.07.001
issn: 1535-6108
e-issn: 1878-3686
Appears in Collections:(IBBTEC) Artículos
(CIB) Artículos
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