ArticleCell cycle (Georgetown, Tex.)2020
Proscillaridin A slows the prostate cancer progression through triggering the activation of endoplasmic reticulum stress.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Harnessing organoid technology in urological cancer: advances and applications in urinary system tumors.World journal of surgical oncology · 2025Review
- The endoplasmic reticulum stress response in prostate cancer.Nature reviews. Urology · 2022Review
- Proscillaridin A induces mitochondrial damage and autophagy in pancreatic cancer and reduces the stability of SMAD4 in Panc-1 cells.Annals of translational medicine · 2022Article
- Research Progress in Pharmacological Activities and Applications of Cardiotonic Steroids.Frontiers in pharmacology · 2022Review
- Cardiac Glycosides as Immune System Modulators.Biomolecules · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PCa) is the second commonly diagnosed malignancy in men over the world. Although androgen deprivation therapy for advanced PCa patients has significantly improved their survival, the majority of these patients eventually develop castration-resistant prostate cancer (CRPC). Proscillaridin A (Pro A), a cardiac glycoside that is clinically used to treat various heart failure diseases, has been reported to have anticancer activity in several cancers. However, whether Pro A exerts an inhibitory effect on PCa progression remains unknown. In this study, we determined possible antitumor effects of Pro A on PCa cells and demonstrated the following: firstly, Pro A selectively inhibited androgen-independent PCa (including PC3 and DU145) cell growth and induced cell apoptosis
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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 OpenQuestion graph.