ArticleFrontiers in pharmacology2026
The pterocarpan (+)-PTC modulates cytoskeletal proteins and induces apoptosis in metastatic castration-resistant prostate cancer: a proteomic perspective.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.