ArticlePloS one2024
Isoscopoletin inhibits hepatocellular carcinoma cell proliferation via regulating glycolysis-related proteins.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIsoscopoletin is one of the primary metabolites of natural product scoparone, which was reported to against tumor proliferation. The aim of this study was to explore the mechanism of isoscopoletin against hepatocellular carcinoma (HCC).
methodsTranscriptomics was used to reveal the possible pathways of isoscopoletin against HCC in vitro. The potential targets of isoscopoletin against HCC through affecting glycolysis were analyzed by network pharmacology, then the potential binding abilities of isoscopoletin to glycolysis-related proteins were initially verified by high throughput virtual molecular docking. The affinities of isoscopoletin for glycolysis-related proteins were assayed using microscale thermophoresis (MST), which was reverse-validated by inhibiting the binding ability of isoscopoletin to GPD2. Glucose consumption and lactate production were examined to evaluate the effects of isoscopoletin on intracellular glycolysis, and the regulation of glycolysis-related targets by isoscopoletin was detected using RT-qPCR and ELISA kits.
resultsThe results of transcriptomics showed that the differentially expressed genes (DEGs) were mainly enriched in glycolysis and other metabolic-related pathways. Network pharmacology and molecular docking revealed that GPD2, GPI, HSP90AA1 and PGK2 were the core targets in the glycolysis process of isoscopoletin against HCC. MST results showed that there was a strong affinity between isoscopoletin and GPD2, GPI, Hsp90α and PGK2. In vitro results showed that isoscopoletin inhibited glucose consumption and lactate production, while regulating the levels of glycolysis-related proteins.
conclusionThis study suggests that isoscopoletin may exist an anti-tumor effect by regulating the glycolysis-related proteins GPD2, GPI, Hsp90α and PGK2, inhibiting the glycolysis process in HCC cells, then blocking the energy supply of tumor cells.
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.