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Updated: Apr 27, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
Published on: March 6, 2018
Icaritin inhibits castration-resistant prostate cancer via RhoB-mediated Akt signaling
Chen Hui1, Zhang Fan2, Ma Yingyao1
1State Key Laboratory of Traditional Chinese Medicine Syndrome, Guangdong Key Laboratory for Translational Cancer Research of Chinese Medicine, International Institute for Translational Chinese Medicine, Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Abstract:
Current therapeutic regimens for castration-resistant prostate cancer (CRPC) are plagued by multiple limitations. RhoB has emerged as a promising molecular target for prostate cancer (PCa) therapy. Icaritin, a bioactive prenylated flavonoid isolated from Epimedii Folium, exhibits potent antitumor and osteogenic properties. However, the anti-CRPC efficacy of icaritin and its underlying molecular mechanisms remain incompletely elucidated. Herein, we evaluated the anti-CRPC potential of icaritin and investigated the involvement of RhoB signaling. Results demonstrated that icaritin significantly suppressed the viability, proliferation, and clonogenic capacity of CRPC cells. Furthermore, in an RM-1 xenograft model, icaritin inhibited tumor growth and reduced serum levels of prostate-specific antigen (PSA) and testosterone. Integrated RNA-seq analysis and The Cancer Genome Atlas-Prostate Adenocarcinoma (TCGA-PRAD) dataset identified RhoB as a candidate therapeutic target in CRPC. Subsequent mechanistic investigations revealed that icaritin inhibits CRPC progression by modulating RhoB-mediated Akt signaling. Collectively, these findings indicate that the anti-CRPC activity of icaritin is at least partially mediated through the RhoB/Akt signaling, providing a pharmacological basis for the further development of icaritin as a potential therapeutic agent against CRPC.
Insights
Icaritin effectively combats castration-resistant prostate cancer (CRPC) by targeting RhoB signaling. This natural compound inhibits tumor growth and proliferation, offering a new therapeutic avenue for prostate cancer (PCa).
Area of Science:
- Oncology
- Pharmacology
- Molecular Biology
Background:
- Castration-resistant prostate cancer (CRPC) presents significant therapeutic challenges.
- RhoB is identified as a key molecular target in prostate cancer (PCa).
- Icaritin, a flavonoid from Epimedii Folium, shows antitumor potential but its anti-CRPC mechanisms are unclear.
Purpose of the Study:
- To evaluate the anti-CRPC efficacy of icaritin.
- To investigate the role of RhoB signaling in icaritin's anti-cancer effects.
- To elucidate the molecular mechanisms underlying icaritin's action against CRPC.
Main Methods:
- In vitro assays assessing CRPC cell viability, proliferation, and clonogenic capacity.
- In vivo RM-1 xenograft model to evaluate tumor growth, PSA, and testosterone levels.
- RNA-sequencing and TCGA-PRAD dataset analysis to identify therapeutic targets.
- Mechanistic studies on RhoB and Akt signaling pathways.
Main Results:
- Icaritin significantly inhibited CRPC cell viability, proliferation, and clonogenic potential.
- In vivo, icaritin suppressed tumor growth and reduced PSA and testosterone levels.
- RhoB was identified as a candidate therapeutic target in CRPC.
- Icaritin modulates RhoB-mediated Akt signaling to inhibit CRPC progression.
Conclusions:
- Icaritin demonstrates significant anti-CRPC activity.
- The anti-tumor effects of icaritin are, in part, mediated by the RhoB/Akt signaling pathway.
- Icaritin shows promise as a potential therapeutic agent for CRPC.
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