Frontiers in pharmacology · 2026
The pterocarpan (+)-PTC modulates cytoskeletal proteins and induces apoptosis in metastatic castration-resistant prostate cancer: a proteomic perspective.
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de Brito Vieira Neto José, Moraes de Farias Kaio, Alves Sales Sarah Leyenne, Melo Vitoria Braga, Nascimento Macêdo Stella Maria, Koscky Paier Carlos Roberto, Bezerra Maria Júlia, Moura Arlindo A, Carvalho Hernandes F, Domingos de Sousa Felipe, Aquino Adriano, de Oliveira Monteiro Ana Cristina, Martins-de-Souza Daniel, Banwell Martin G, Miranda Furtado Cristiana Libardi, Pessoa Claudia
Аннотация
Treatment of metastatic, castration-resistant prostate cancer (mCRPC) remains clinically challenging due to tumor heterogeneity and resistance to standard microtubule-targeting agents, such as docetaxel and cabazitaxel. The natural pterocarpan (+)-(6aS,11aS)-2,3,9-trimethoxypterocarpan [(+)-PTC] has previously shown selective cytotoxicity and disruption of bipolar spindle assembly in mCRPC PC-3 cells yet its full mechanism of action and global proteomic impact remain uncharacterized. PC-3 cells were treated with (+)-PTC (2.0 µM or 8.0 µM) for 24 h and assessed by flow cytometry (Annexin V and rhodamine 123) Western blot, and caspase-3/7 luminescence assays. Global proteomic profiling was performed by quantitative LC-MS/MS using a 2D nano-UPLC data-independent acquisition platform with nocodazole (0.25 µM, microtubule depolymerizer) and monastrol (50 µM, Eg5 inhibitor) as comparators. (+)-PTC-induced concentration-dependent apoptosis (19.8% early apoptotic cells at 2.0 µM; 26.1% at 8.0 µM) and progressive mitochondrial membrane depolarization. Western blot and caspase activities assays confirmed upregulation of BAX and caspase-7, consistent with intrinsic pathway activation. Proteomic analysis identified 212 differentially expressed proteins (DEPs) in (+)-PTC-treated cells, with over 80% overlap with nocodazole-treated cells (82% among upregulated and 84% among downregulated proteins), while clustering with monastrol was markedly lower. The top upregulated proteins, TTLL3, ANAPC7, PIK3CA, ARID4B, and COL16A1, are linked to microtubule dynamics and cell cycle regulation; the main downregulated, namely KDM2B, PTOV1, YWHAQ, PSMB6, and PRKCB, are involved in cell survival, protein homeostasis and mitotic checkpoint control. These findings provide proteomic evidence that (+)-PTC interferes with cytoskeletal protein dynamics and promotes apoptosis in mCRPC and so warranting its further investigation as a candidate anti-cancer scaffold.