ArticleJournal of translational medicine2026
Palbociclib targets β-catenin for degradation and synergizes with KRAS or ERK5 inhibition in colorectal cancer preclinical models.
Article in Journal of translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundColorectal cancer (CRC) is a leading cause of cancer-related mortality, largely driven by aberrant activation of the WNT/β-catenin and RAS pathways. Despite recent therapeutic advances, effective strategies to target these oncogenic signals remain limited.
methodsA multi-step chemical library screen was performed to identify compounds capable of suppressing β-catenin and RAS signaling. Drug mechanisms and combination effects were investigated through functional assays, in vitro and in vivo experiments, and transcriptomic profiling. Survival analysis of the Sidra-LUMC AC-ICAM CRC cohort (n = 303) was conducted to evaluate the prognostic significance of candidate target genes.
resultsWe identified the CDK4/6 inhibitor palbociclib as an unexpected suppressor of β-catenin signaling. Uniquely, palbociclib promoted GSK3β-mediated β-catenin degradation by dampening AKT activity, revealing a previously unrecognized mechanism of action and broadening its role beyond canonical cell-cycle inhibition. Building on this mechanism, we found that combining palbociclib with the KRAS
conclusionsTogether, these findings position palbociclib as a versatile therapeutic backbone in CRC. By simultaneously targeting cell cycle and oncogenic signaling networks, palbociclib-based combinations induce synergistic and durable responses, offering a compelling rationale for tailored therapeutic strategies in molecularly defined CRC.
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