ArticleAmerican journal of translational research2025
Targeting the FoxJ3/FoxO6 axis suppresses hepatocellular carcinoma growth by inducing cell cycle arrest and apoptosis.
Article in American journal of translational 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
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the biological function of Forkhead box J3 (FoxJ3) in hepatocellular carcinoma (HCC).
methodsFoxJ3 expression in HCC was analyzed using next-generation sequencing, and its association with overall survival and other Fox family proteins was evaluated. The biological roles of FoxJ3 and its relationship with Fox family members were investigated in vitro through MTT, cell cycle, and apoptosis assays. A xenograft model was established to assess the effects of FoxJ3 knockdown on tumor growth.
resultsFoxJ3 expression was significantly upregulated in HCC tissues, which was associated with poor prognosis and survival. Among Fox proteins family, forkhead box O6 (FoxO6) showed the strongest correlation with FoxJ3 expression. Furthermore, FoxJ3 knockdown suppressed the HCC cell proliferation in vitro and inhibited tumor growth in vivo. Mechanistically, FoxJ3 knockdown induced cell-cycle arrest and apoptosis, as demonstrated by decreased expression of PCNA, Ki67, Bcl-2, CDK4, and cyclin D1, alongside increased Bax and the activation of key apoptotic executers, cleaved caspase-3 and cleaved PARP. Moreover, FoxJ3 knockdown reduced the expression of FoxO6.
conclusionsFoxJ3 may act as an oncogene in HCC via regulating FoxO6. Its knockdown inhibits HCC cell proliferation mainly via cell-cycle arrest and apoptosis induction. FoxJ3/FoxO6 axis may represent a novel therapeutic target for HCC.
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.