ArticleTranslational cancer research2023
Effects of p-cresol, a uremic toxin, on cancer cells.
Article in Translational cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Untargeted Metabolomics Reveals Metabolic Reprogramming Linked to HCC Risk in Late Diagnosed Tyrosinemia Type 1.Metabolites · 2025Article
- Targeting cancer metabolism through p-cresol mediated Inhibition of pyruvate dehydrogenase kinase 3 in lung cancer.Scientific reports · 2025Article
- UnravelingFrontiers in pharmacology · 2025Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Though p-cresol exists at a low concentration in the blood, it accumulates in various organs of uremic patients. Previous research has shown that the p-cresol promoted bladder cancer cell invasion and migration. This study aims to see if p-cresol had similar effects on kidney cancer cells and liver cancer cells. Methods: For 48 hours, 786-O human renal cancer cells and HepG2 human liver cancer cells were treated with p-cresol at concentrations of 0, 10, 20, 40, and 70 µM. The effects of p-cresol on cell viability, apoptosis, migration, and invasion were then analyzed using the CCK-8, TUNEL, and Transwell migration/invasion assays, respectively. Results: P-cresol at 0 to 70 µM for 48 hours had no significant toxic effects on 786-O cells or HepG2 cells. We chose 40 µM p-cresol for 48 hours for the following experiment. The viability and proliferation of 786-O cells and HepG2 cells were unaffected after 48 hours of treatment, with 40 µM p-cresol. However, 40 µM p-cresol for 48 hours promoted HepG2 cell migration and invasion but did not have the same effect on the 786-O cell line. Conclusions: P-cresol may be responsible for HepG2 cells' malignant biological behavior. Because the liver is the primary site of p-cresol metabolism, it is important to study the responses of cancer cells in the liver to p-cresol.
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