ArticleDiscover oncology2025
Identification of potential molecular targets of luteolin in the treatment of hepatocellular carcinoma based on network pharmacology and transcriptome sequencing technology.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
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
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
- Global research landscape and multisystem health mechanisms of luteolin: a comprehensive bibliometric and network pharmacology study.Frontiers in nutrition · 2026Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
objectiveThis study aims to identify potential target genes of luteolin (LUT) for treating hepatocellular carcinoma (HCC) through integrated in vitro experiments, network pharmacology, bioinformatics, and transcriptome sequencing (RNA-seq).
methodsPotential LUT-associated therapeutic targets for HCC were predicted using network pharmacology. The anti-HCC effects of LUT were evaluated in vitro by assessing its impact on SMMC-7721 and HepG2 cell viability, apoptosis, migration, and invasion. Transcriptome sequencing was performed to identify differentially expressed genes (DEGs) in LUT-treated HepG2 cells, followed by bioinformatics analyses to validate hub targets and their associated pathways.
resultNetwork pharmacology predicted 100 potential protein targets of LUT for HCC treatment, implicating pathways related to inflammation, cell migration, cell cycle regulation, and apoptosis, including the HIF-1α signaling axis. In vitro experiments demonstrated that LUT (40, 60, and 90 µmol·L
conclusionLLUT suppresses HCC progression by inhibiting proliferation, regulating cell cycle and apoptosis, and blocking invasion and migration. Its therapeutic mechanisms likely involve targeting MMP9 and modulating the HIF-1α signaling pathway.
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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 OpenQuestion graph.