ArticleInternational journal of medical sciences2026
Activation of the Hippo Pathway by ATN Suppresses Cancer Stem-Like Properties and EGFR-Associated Signaling in Castration-Resistant Prostate Cancer Cells
Article in International journal of medical sciences, 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
Background: Castration-resistant prostate cancer (CRPC) represents a lethal stage of prostate cancer for which effective therapeutic options remain limited. Aberrant activation of the Hippo pathway effector Yes-associated protein (YAP) and its crosstalk with epidermal growth factor receptor (EGFR) signaling have been implicated in tumor progression, cancer stemness, and metastasis. This study aimed to investigate the therapeutic potential and underlying mechanisms of ATN, a 1,2,4-oxadiazole-based YAP inhibitor, in CRPC cells. Methods: The anti-cancer activity of ATN was evaluated in CRPC cell lines, PC3 and DU145, using cell viability, colony formation, apoptosis, tumorsphere, and transwell migration assays. Western blotting and immunofluorescence analyses were performed to assess Hippo-YAP and EGFR signaling pathways. Functional rescue experiments were conducted using YAP overexpression and constitutively active Akt (CA-Akt). Results: ATN significantly suppressed CRPC cell viability in a concentration-dependent manner, with IC₅₀ values of 1.13 μM for PC3 cells and 0.43 μM for DU145 cells, while exhibiting lower cytotoxicity toward non-tumorigenic fibroblasts (IC₅₀ = 1.72 μM). Mechanistically, ATN increased YAP phosphorylation at Ser397, promoted its degradation, and reduced nuclear YAP localization. This was accompanied by downregulation of YAP target proteins, including c-Myc and NFκB. Functionally, ATN significantly inhibited proliferation, induced apoptosis, and suppressed tumorsphere formation and CD44 Conclusion: ATN exerts potent anti-tumor effects against CRPC cells by activating the Hippo pathway, promoting YAP degradation, and disrupting the YAP-associated EGFR signaling network. These findings highlight ATN as a promising therapeutic candidate for targeting YAP-driven oncogenic signaling in CRPC.
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