ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Integrative systems biology and transcriptomic database analysis (GEPIA2 and TNMplot) uncover HRAS-driven anticancer mechanisms of anthraquinones in liver cancer.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver cancer, primarily hepatocellular carcinoma (HCC), remains a major contributor to global cancer mortality, underscoring the need for effective targeted therapies. This study employed an integrative systems biology and transcriptomic approach to investigate the anticancer potential of anthraquinones targeting HRAS in liver cancer. Putative targets of anthraquinones were predicted using Digep-Pred, while liver cancer-associated genes were retrieved from GeneCards, yielding 215 overlapping targets. Protein-protein interaction (PPI) network analysis identified key hub genes, including AKT1, TP53, and HRAS. Gene Ontology and KEGG pathway enrichment analyses revealed significant involvement of PI3K-Akt, MAPK, and Ras signaling pathways, highlighting their roles in tumor progression and therapeutic modulation. Network pharmacology further established HRAS as a central regulatory node. Pan-cancer transcriptomic profiling using GEPIA2 and TNMplot demonstrated significant overexpression and dysregulation of HRAS across multiple cancers, including liver cancer, with strong associations to tumor progression and prognosis. Genomic analysis via cBioPortal revealed mutation hotspots and copy-number-dependent expression patterns influencing HRAS activity. Molecular docking studies indicated that anthraquinones, particularly citreorosein, exhibited strong binding affinity (- 7.431) toward the HRAS active site through key interactions with SER17, LYS16, GLY13, THR35, and GLU31, outperforming standard drugs such as sorafenib. Molecular dynamics simulations confirmed the stability of the HRAS-citreorosein complex, with low RMSD values indicating minimal conformational deviation and stable binding. Dynamic cross-correlation analysis revealed coordinated residue motions and balanced correlated anticorrelated dynamics, supporting structural integrity. Collectively, these findings highlight HRAS as a promising therapeutic target and anthraquinones as potential candidates for liver cancer treatment.
Indexed as
Identifiers
42484860What OpenQuestion holds
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.