ArticleJournal of hepatocellular carcinoma2026
Aberrant Cholesterol Metabolism Caused by Decreased Lecithin: Cholesterol Acyltransferase Promoted Hepatocarcinogenesis.
Article in Journal of hepatocellular carcinoma, 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
No grant is acknowledged in the PubMed record.
Abstract
Background: Hepatocellular carcinoma (HCC), the most common primary liver cancer, exhibits metabolic reprogramming with disrupted cholesterol metabolism as a key feature. Lecithin-cholesterol acyltransferase (LCAT) contributes to HCC development, but its exact on cogenic mechanisms remain unclear. This study aims to investigate the role of LCAT in hepatocarcinogenesis and elucidate its underlying molecular mechanisms in HCC. Methods: The Cancer Genome Atlas (TCGA), GEPIA, and Kaplan-Meier plotter databases were used to analyze LCAT expression and perform survival analysis and functional enrichment analysis. Clinical paired samples were collected to evaluate LCAT expression and observed changes in cholesterol metabolism levels Liver-specific Results: LCAT expression level was down-regulated in HCC patients and low LCAT level was associated with poor prognosis. International Cancer Genome Consortium (ICGC) data reveal dysregulated cholesterol metabolism in HCC, further validated by clinical evidence of metabolic aberrations in patients Besides, we constructed DEN induced HCC model using Conclusion: This study first explored the biological functions of LCAT in HCC based on in vitro and in vivo experiments. Our results indicate that LCAT deficiency correlates with aggressive HCC progression and immunosuppression, suggesting its potential as a prognostic biomarker. Given its role in modulating the HCC microenvironment, LCAT warrants further investigation as a predictive marker for immunotherapy response.
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.