ArticleCancer cell international2026
CDK4 inhibition by luteolin enhances lenvatinib sensitivity in HCC via Wnt/β-catenin modulation.
Article in Cancer cell international, 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
6 authors.
Funding
Abstract
backgroundHepatocellular carcinoma (HCC) frequently develops resistance to lenvatinib. We investigated CDK4’s role in this resistance and the potential of Danshen/luteolin to overcome it.
methodsUsing bioinformatics, in vitro models, and in vivo xenografts, we modulated CDK4 expression (overexpression/shRNA) in HCC cells. Danshen extract and luteolin’s effects on lenvatinib sensitivity were assessed via viability/apoptosis assays and molecular analyses. Wnt/β-catenin pathway involvement was tested with an inhibitor and luciferase reporter.
resultsNetwork pharmacology identified CDK4 as a Danshen target in resistant HCC. High CDK4 correlated with poor prognosis and increased resistance. Danshen/luteolin reduced CDK4 protein, enhanced lenvatinib sensitivity, and suppressed tumor growth in vitro and in vivo. Luteolin promoted CDK4 degradation via the ubiquitin-proteasome pathway and modulated Wnt/β-catenin signaling, crucial for resistance.
conclusionsCDK4 is a key mediator of lenvatinib resistance in HCC. Danshen-derived luteolin acts as a CDK4 inhibitor, enhancing lenvatinib sensitivity by degrading CDK4 and targeting Wnt/β-catenin, supporting combination therapies to overcome resistance.
Indexed as
Identifiers
What 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.