ArticleAnnals of surgical oncology2025
ARID4B Promotes the Progression of Hepatocellular Carcinoma Through the PI3K/AKT Pathway.
Article in Annals of surgical oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed.
- Clinical and Functional Impact of CHMP3 in Pancreatic Ductal Adenocarcinoma.Annals of surgical oncology · 2026Article
- Article
- Mitochondrial-related biomarkers as the diagnostic markers in sepsis induced acute respiratory distress syndrome.European journal of medical research · 2026Article
- Stereotactic body radiation therapy for hepatocellular carcinoma: a comprehensive review.Frontiers in oncology · 2026Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
backgroundAT-rich interaction domain 4B (ARID4B) is a transcriptional activator that regulates the phosphatidylinositol 3-kinase (PI3K)/AKT pathway in prostate cancer. However, the role of ARID4B in hepatocellular carcinoma (HCC) has remained unclear.
methodsThis study included 162 patients who had undergone primary hepatic resection for HCC between 2008 and 2019. Their HCC samples were immunohistochemically stained for ARID4B, and ARID4B score was calculated from the intensity and percentage of staining. We retrospectively investigated the association of ARID4B score with disease-free and overall survival, and primary recurrence patterns of HCC. Furthermore, human HCC cell lines (HuH-1 and HuH-7) were knocked down for ARID4B using small-interfering RNA (siRNA), and the expression of PI3K/AKT proteins, cell proliferation, migration, and invasion ability were assessed.
resultsIn multivariate analyses, negative HBs-antigen (p = 0.02), multiple tumors (p < 0.01), microvascular invasion (p = 0.03), and high ARID4B score (p = 0.01) were independent predictors of disease-free survival, while tumor size >5 cm (p = 0.03), microvascular invasion (p < 0.01), and high ARID4B score (p = 0.04) were independent predictors of overall survival. A high ARID4B score was associated with high serum α-fetoprotein (AFP) level (p = 0.04), poor tumor differentiation (p < 0.01), and microvascular invasion (p < 0.01). ARID4B scores were significantly lower in the no recurrence, intrahepatic recurrence, and extrahepatic recurrence groups, in that order. Knockdown of ARID4B using siRNA in human HCC cell lines significantly suppressed the PI3K/AKT pathway, cell proliferation, migration, and invasion.
conclusionsARID4B may activate the PI3K/AKT signaling pathway in HCC and may be a prognostic factor after hepatic resection for HCC.
Indexed as
Identifiers
39751985What 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.