ArticleiScience2026
CDC20 promotes prostate cancer progression via modulating c-MYC and PI3K-AKT signaling.
Article in iScience, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer shows substantial variability in clinical outcomes, underscoring the need for reliable biomarkers and mechanistic insights. Analysis of The Cancer Genome Atlas data identified CDC20 as an independent prognostic factor with elevated expression in prostate cancer. Functional studies in DU145 and PC-3 cells demonstrated that CDC20 promotes cell proliferation, migration, invasion, and cell cycle progression. Co-immunoprecipitation and loss-of-function analyses indicated that CDC20 interacts with c-MYC and influences PI3K-AKT signaling. In a xenograft model, CDC20 knockdown reduced tumor growth, whereas its overexpression enhanced tumor progression. These findings suggest that CDC20 contributes to prostate cancer progression, at least in part, through a c-MYC-associated PI3K-AKT signaling axis, and support its potential relevance for prognostic assessment and therapeutic targeting.
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Registered trials
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