ArticleTranslational cancer research2025
FBXO5 drives hepatocellular carcinoma progression and is a target for tea polyphenol-mediated inhibition.
Article in Translational cancer research, 2025. 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
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Hepatocellular carcinoma (HCC) ranks among the leading causes of cancer-related deaths globally, with current treatments offering limited efficacy. FBXO5 has emerged as a potential oncogene in multiple cancers, yet its role in HCC remains incompletely understood. Notably, tea polyphenols (TPs) are natural compounds with known antitumor properties, but their molecular targets in HCC remain unclear. This study aims to investigate the role of FBXO5 in HCC and explore whether TPs exert their antitumor effects by targeting FBXO5. Methods: FBXO5 expression in HCC was analyzed using The Cancer Genome Atlas (TCGA) data. Functional analysis of FBXO5 in HCC cell lines was performed using small interfering RNA (siRNA) knockdown and overexpression techniques. Cell phenotypes were assessed via Cell Counting Kit-8 (CCK-8), colony formation, scratch healing, and Transwell assays. Cells treated with varying concentrations of TPs were evaluated for effects on viability, proliferation, migration, and invasion, with FBXO5 expression changes analyzed by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot. TPs' effects were further validated in FBXO5-overexpressing cells. Results: FBXO5 was significantly upregulated in HCC tissues and correlated with poor patient prognosis. Silencing FBXO5 inhibited HCC cells proliferation, migration, and invasion, whereas its overexpression promoted these malignant behaviors. TPs treatment dose-dependently suppressed HCC cells viability, proliferation, and motility. TPs downregulated FBXO5 expression at both messenger RNA (mRNA) and protein levels. Overexpression of FBXO5 attenuated the antitumor effects of TPs, indicating that TPs partially inhibit HCC progression by suppressing FBXO5. Conclusions: FBXO5 functions as an oncogene in HCC, and TPs may serve as potential therapeutic agents for inhibiting HCC progression by targeting FBXO5.
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.