ArticleAnnals of translational medicine2022
Proscillaridin A induces mitochondrial damage and autophagy in pancreatic cancer and reduces the stability of SMAD4 in Panc-1 cells.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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
2 citing papers in PubMed.
- Policosanol alleviates chronic stress-induced growth impairment via gut microbiota-metabolite interactions: insights from 16S rRNA sequencing and LC-MS metabolomics.Frontiers in nutrition · 2025Article
- Cytotoxic and Pro-Apoptotic Effects of Leaves Extract ofMolecules (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pancreatic cancer (PC) is a highly metastatic and lethal cancer with a very low overall 5-year survival rate. There is an urgent need for identifying new therapeutic agents for this deadly disease. Cardiac glycosides (CGs) have been traditionally used for their potent cardiovascular activities and have also recently been reported to exhibit anti-tumor effects. Proscillaridin A (Pro A), a natural CG, has been shown to display anti-tumor effects on multiple cancer types. Methods: The cytotoxic effect of Pro A on PC cells was determined using cell viability assay, colony formation assay and transwell assay Results: Pro A inhibits the proliferation, migration and invasion of Panc-1, BxPC-3 and AsPC-1 PC cells Conclusions: Our findings suggest that Pro A constitutes a promising therapeutic candidate for certain types of PC.
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