ArticleAging2022
A comprehensive analysis of FOX family in HCC and experimental evidence to support the oncogenic role of FOXH1.
Article in Aging, 2022. 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
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- FOXP1 transcriptionally activates NUSAP1 to induce M2 polarization of tumor-associated macrophages via glycolysis in hepatocellular carcinoma.Frontiers in genetics · 2026Article
- Zebrafish model of palmitic acid induced MAFLD recapitulates pathways conserved in mice and humans.Scientific reports · 2025Article
- Targeting the FoxJ3/FoxO6 axis suppresses hepatocellular carcinoma growth by inducing cell cycle arrest and apoptosis.American journal of translational research · 2025Article
- CAF-EVs carry lncRNA MAPKAPK5-AS1 into hepatocellular carcinoma cells and promote malignant cell proliferation.Communications biology · 2024Article
- Transforming growth factor-β (TGF-β) signaling pathway-related genes in predicting the prognosis of colon cancer and guiding immunotherapy.Cancer pathogenesis and therapy · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) remains the second leading cause of cancer related deaths worldwide. Understanding about the molecular biology of HCC and development of targeted therapies are still the main focuses of this type of disease. Here, by connecting the expression levels of FOX proteins with their associated clinical characteristics using TCGA LIHC dataset, we found that 27/40 FOX proteins were highly expressed in HCC tumors compared to normal liver tissues and their expression levels were tightly associated with HCC tumor stage, tumor grade and overall survival. Our experimental results also confirmed that FOXH1 indeed played an oncogenic role in HCC development by promoting cell growth and cell migration/invasion. Mechanistic dissection demonstrated that FOXH1-induced cell growth and cell migration/invasion relied on mTOR signaling because inhibition of mTOR signaling by rapamycin could attenuate FOXH1-mediated phenotypic alterations of HCC cells. The results from orthotopic mouse model also validated that FOXH1 promoted HA22T tumor growth via triggering mTOR activation. Overall, this study not only comprehensively examines the clinical values of FOX proteins in HCC but also provides experimental evidence to support the role of FOXH1 in HCC development, building rationale to develop more effective therapies to treat HCC patients.
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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.