ArticleBMC gastroenterology2026
FBXW8 is upregulated in hepatocellular carcinoma and promotes HCC cell malignancy.
Article in BMC gastroenterology, 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
aimInvestigate FBXW8 expression levels in hepatocellular carcinoma (HCC), its biological roles and prognostic significance.
methodsBased on the analysis of The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus databases, the expression level of FBXW8 was investigated. The results were verified in clinical samples using quantitative polymerase chain reaction (qPCR) and immunohistochemistry (IHC). Functional experiments (Cell Counting Kit-8, wound healing, and Transwell) were conducted on Huh7 and MHCC-97 H cells. Immune infiltration and methylation status were also evaluated.
resultsFBXW8 was significantly overexpressed in HCC tissues across multiple cohorts (TCGA, GSE25097, GSE54236; all p < 0.001), with consistent validation by qPCR and IHC in clinical specimens. Elevated FBXW8 expression correlated with aggressive clinicopathological characteristics, specifically, advanced tumor-node-metastasis staging, poor histological grade, and higher alpha-fetoprotein levels (all p < 0.05). High FBXW8 expression was associated with worse overall survival (hazard ratio [HR] = 1.52, p = 0.024), with Progression-free interval (HR = 1.45, p = 0.013) also adversely affected. Receiver operating characteristic analysis demonstrated that FBXW8 had diagnostic value. The areas under the curve in the TCGA, GSE25097 and GSE54236 datasets were 0.875, 0.837 and 0.716, respectively. The in vitro functional experiments demonstrated that FBXW8 overexpression promoted cell proliferation, migration, and invasion (all p < 0.05). The FBXW8 expression was positively correlated with T helper cells (r = 0.342), while it was negatively correlated with dendritic cells (r = - 0.379). Promoter hypermethylation of FBXW8 was observed in HCC, with three CpG sites associated with prognosis.
conclusionFBXW8 functions as a prognostic biomarker and promotes HCC progression, indicating its therapeutic potential.
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.