ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Integrated experimental and network pharmacology analyses reveal inhibitory effects of albiflorin on renal cell carcinoma cells.
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
8 authors.
Funding
Abstract
Renal cell carcinoma (RCC) remains a clinically challenging malignancy because of its marked molecular heterogeneity and the limited long-term efficacy of current systemic therapies. Albiflorin, a major bioactive constituent of Paeonia lactiflora, has been reported to possess anti-inflammatory, antioxidant, and cytoprotective activities, whereas its potential role in RCC remains unclear. In the present study, the anti-RCC activity of albiflorin was investigated by integrating in vitro experiments, network pharmacology, and molecular docking, and experimental validation. CCK-8 assays showed that albiflorin reduced the viability of 786-O and A498 cells in a concentration-dependent manner, with lower IC50 values in RCC cells than in HK-2 cells. EdU incorporation and wound-healing assays further demonstrated that albiflorin suppressed RCC cell proliferation and migration. Albiflorin-related targets were collected from SuperPred and SwissTargetPrediction, while RCC-related targets were obtained from the KICH, KIRC, and KIRP datasets in TCGA. Sixty-four overlapping targets were identified. GO and KEGG enrichment analyses indicated that these targets were mainly associated with signal transduction, apoptosis, migration, angiogenesis, and cancer-related pathways, including MAPK, PI3K-Akt, Ras, and calcium signaling. Candidate target screening identified EGFR, MMP9, and FGF2 as representative candidate targets. Molecular docking supported the potential binding of albiflorin to EGFR and MMP9. RT-qPCR showed that albiflorin reduced MMP9 and FGF2 mRNA expression, whereas EGFR mRNA was not markedly altered. Western blotting showed decreased EGFR and ERK phosphorylation, and EGF stimulation partially restored EGFR/MAPK signaling activation in albiflorin-treated RCC cells. These findings suggest that albiflorin inhibits RCC cell viability, proliferation, and migration, partly through suppression of EGFR/MAPK signaling and regulation of tumor progression-related molecules.
Indexed as
Identifiers
42201344What 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.