CDC20 promotes prostate cancer progression via modulating c-MYC and PI3K-AKT signaling

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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Publication Details

Journal
iScience
Published
2026-06-18
DOI
https://doi.org/10.1016/j.isci.2026.116409
Primary Topic
Prostate Cancer Treatment and Research
Type
article
Field-Weighted Citation Impact
0.00

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article

CDC20 promotes prostate cancer progression via modulating c-MYC and PI3K-AKT signaling

Zhenyu Fu, Xinyu Xu, Chaozhong Wang, Jing Zhai et al.
iScience
Prostate Cancer Treatment and Research
article

CDC20 promotes prostate cancer progression via modulating c-MYC and PI3K-AKT signaling

Zhenyu Fu, Xinyu Xu, Chaozhong Wang, Jing Zhai, Wenhui Zhu, Ke Lu, Jixiang Ding, Yizhou Wang, Jiaojiao Chen, Ningning Zhang
article en

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.

iScienceVol. 29(7)
Nantong University (CN), Fudan University (CN), Affiliated Hospital of Nantong University (CN), Shanghai University of Traditional Chinese Medicine (CN), Changshu No.1 People's Hospital (CN), Yueyang Hospital (CN), Huashan Hospital (CN)
Jiangsu Provincial Commission of Health and Family Planning
Good health and well-being
Openalex Percentile: Top 8%
Prostate Cancer Treatment and Research
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