ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Stachydrine hydrochloride induces cell senescence and ferroptosis of castration-resistant prostate cancer.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Stachydrine: A Systematic Review of Its Multi-Targeted Therapeutic Potential in Cardiovascular, Oncology, Renal, Gynecological, and Inflammatory Disorders.Drug design, development and therapy · 2026Pooled it
- Programmed cell death mechanisms of traditional plant medicine in prostate cancer therapy.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Paclitaxel resistance of castration-resistant prostate cancer (CRPC) remains a substantial challenge in clinical oncology. Our investigation aimed to explore the potential of stachydrine hydrochloride in addressing paclitaxel resistance within CRPC. Parental prostate cancer cells, PC3 and DU145, and the corresponding paclitaxel-resistant counterparts, PC3-TxR and DU145-TxR, were subjected to indicated concentrations to determine the IC50 of paclitaxel and stachydrine hydrochloride. Cell viability and proliferation were evaluated by MTT and colony formation assays. Stachydrine hydrochloride-mediated apoptosis, senescence, and ferroptosis were detected using Western blot, SA-β-gal staining, and QuantiChrom iron assay. We found a pronounced reduction in paclitaxel resistance in both PC3-TxR and DU145-TxR cells following exposure to stachydrine hydrochloride. The considerable decrease in paclitaxel's IC50 values in these cells highlights the potential of stachydrine hydrochloride in sensitizing CRPC cells to paclitaxel-based therapies. Mechanistically, stachydrine hydrochloride treatment significantly upregulated the expression of estrogen receptor beta (ERβ) and promoted cell apoptosis, senescence, and ferroptosis pathways in CRPC. Our study provides promising insights into the potential of stachydrine hydrochloride as a novel therapeutic adjunct in overcoming paclitaxel resistance in CRPC.
Indexed as
Identifiers
40266302What 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.