ArticleHeliyon2024
Nitidine chloride inhibits G2/M phase by regulating the p53/14-3-3 Sigma/CDK1 axis for hepatocellular carcinoma treatment.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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
3 citing papers in PubMed.
- Discovery of Benzophenanthridine Alkaloids fromPharmaceuticals (Basel, Switzerland) · 2026Article
- Alkaloids mediated regulation of microRNA in cancer: molecular insights and emerging therapeutic strategies.Frontiers in oncology · 2026Review
- Kaempferol triggers cellular senescence via CDK1 ubiquitination in HCC cells.Cancer cell international · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Liver cancer had become the sixth most common cancer. Nitidine chloride (NC) has demonstrated promising anti-HCC properties; however, further elucidation of its mechanism of action is necessary. Methods: The anti-HCC targets of NC were identified through the utilization of multiple databases and ChIPs data analysis. The GO and KEGG analyses to determine the specific pathway affected by NC. The Huh 7 and Hep G2 cells were subjected to a 24-h treatment with NC, followed by evaluating the impact of NC on cell proliferation and cell cycle. The involvement of the p53/14-3-3 Sigma/CDK1 axis in HCC cells was confirmed by qPCR and WB analysis of the corresponding genes and proteins. Results: The GO and KEGG analysis showed the targets were related to cell cycle and p53 signaling pathways. In vitro experiments showed that NC significantly inhibited the proliferation of HCC cells and induced G2/M phase arrest. In addition, qPCR and WB experiments showed that the expression of p53 in HCC cells increased after NC intervention, while the expression of 14-3-3 Sigma and CDK1 decreased. Conclusion: NC can inhibit the proliferation of HCC cells and induce G2/M cell cycle arrest, potentially by regulating the p53/14-3-3 Sigma/CDK1 axis
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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 Socratic graph.