ArticleJournal of biosciences2017
Cytotoxic and toxicogenomic effects of silibinin in bladder cancer cells with different TP53 status.
Article in Journal of biosciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 30 citations in OpenAlex.
- Milk Thistle (Current medicinal chemistry · 2025Review
- A comprehensive evaluation of the therapeutic potential of silibinin: a ray of hope in cancer treatment.Frontiers in pharmacology · 2024Review
- Properties of flavonoids in the treatment of bladder cancer (Review).Experimental and therapeutic medicine · 2022Review
- The Role of Epigenetic Modifications in Human Cancers and the Use of Natural Compounds as Epidrugs: Mechanistic Pathways and Pharmacodynamic Actions.Biomolecules · 2022Review
- Global Trends in Research of Treatment on Bladder Cancer with Chinese Medicine Monomer from 2000 to 2021: A Bibliometric Analysis.Journal of oncology · 2022Article
- Cytotoxic potentials of silibinin assisted silver nanoparticles on human colorectal HT-29 cancer cells.Bioinformation · 2020Article
- Traditional Chinese medicine as a cancer treatment: Modern perspectives of ancient but advanced science.Cancer medicine · 2019Review
- Silibinin inhibits the migration and invasion of human gastric cancer SGC7901 cells by downregulating MMP-2 and MMP-9 expression via the p38MAPK signaling pathway.Oncology letters · 2017Article
- Role of Silymarin in Cancer Treatment: Facts, Hypotheses, and Questions.Journal of evidence-based integrative medicineReview
- Huaier Inhibits Proliferation, Migration, and Invasion of Cutaneous Squamous Cell Carcinoma Cells by Inhibiting the Methylation Levels of CDKN2A and TP53.Integrative cancer therapiesArticle
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silibinin is a natural phenol found in the seeds of the milk thistle plant. Recent data have shown its effectiveness for preventing/treating bladder tumours. Therefore, in this study we investigated the cytotoxic and toxicogenetic activity of silibinin in bladder cancer cells with different TP53 statuses. Two bladder urothelial carcinoma cell lines were used: RT4 (wild-type TP53 gene) and T24 (mutated TP53 gene). Cell proliferation, clonogenic survival, apoptosis rates, genotoxicity and relative expression profile of FRAP/mTOR, FGFR3, AKT2 and DNMT1 genes and of miR100 and miR203 were evaluated. Silibinin promoted decreased proliferation and increased late apoptosis in TP53 mutated cells. Increased early apoptosis rates, primary DNA damage, and decrease of cell colonies in the clonogenic survival assay were detected in both RT4 and T24 cell lines. Down-regulation of FRAP/mTOR, AKT2, FGFR3, DNMT1 and miR100 expression occurred in RT4 cells. Modulation of miR203 was observed in both cell lines. In conclusion, despite the reduction of clone formation in both cell lines, the toxicogenomic effect of silibinin on FRAP/mTOR, AKT2, FGFR3, DNMT1 and miR100 was dependent on the TP53 status. Taken together, the data confirmed the role of silibinin as an antiproliferative compound, whose mechanism of action was related to the TP53 status.
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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.