ArticleFrontiers in molecular biosciences2026
TUBB2A expression and its prognostic significance in hepatocellular carcinoma revealed by cholesterol-metabolism-related gene profiling.
Article in Frontiers in molecular biosciences, 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
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Hepatocellular carcinoma (HCC) exhibits significant molecular heterogeneity and is associated with a poor prognosis. The lack of validated biomarkers limits early diagnosis and effective prognosis. Identifying oncogenic drivers in HCC may enhance risk stratification and provide new therapeutic targets. Recent evidence links disrupted cholesterol metabolism to hepatic oncogenesis, and a comprehensive profiling of cholesterol-related genes may help identify metabolic oncogenic signatures and prognostic biomarkers for HCC. Methods: Bioinformatic analyses were performed using public databases to assess differential expression and the prognostic significance of TUBB2A. Gene set enrichment analysis (GSEA) was conducted to identify key biological pathways associated with TUBB2A expression in HCC. These findings were validated through RT-qPCR, Western blot, and immunohistochemistry on patient tissues. Functional studies included siRNA knockdown and plasmid overexpression in HCC cell lines, followed by assays for cellular proliferation, clonogenicity, migration, and invasion. Tumorigenicity was tested using xenograft models in nude mice. The prognostic value of TUBB2A was evaluated through survival curves and time-dependent ROC analysis. Results: TUBB2A was identified as a dysregulated and prognostically significant biomarker in HCC through bioinformatic analyses. Pathway analysis using databases like KEGG, GOBP, and Hallmark revealed significant enrichment of TUBB2A in pathways related to cholesterol metabolism, fatty acid biosynthesis, and steroid biosynthesis. Experimental validation demonstrated that TUBB2A is overexpressed in HCC tissues and cell lines. Elevated TUBB2A expression correlated with higher AFP levels, microvascular invasion, advanced tumor stages, and poorer overall survival. Functional assays showed that knockdown of TUBB2A suppressed proliferation, migration, invasion, and Discussion: TUBB2A plays a key role in promoting HCC tumorigenesis and is associated with adverse clinical outcomes. The integration of bioinformatic analyses and experimental validation establishes TUBB2A as a potential prognostic biomarker in HCC. Its role in regulating cholesterol metabolism suggests that TUBB2A may be a novel target for therapeutic interventions. Further studies should explore the clinical utility of TUBB2A, including its integration into multi-marker models and as a target for targeted therapy, offering potential avenues to improve HCC treatment strategies.
Indexed as
Identifiers
What Socratic 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 Socratic graph.