ArticleOxidative medicine and cellular longevity2022
HNF4A Regulates the Proliferation and Tumor Formation of Cervical Cancer Cells through the Wnt/
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- HNF4α-HKDC1 axis orchestrates a metabolic rewiring to promote migration and metastasis in advanced gastric cancer.Cell death & disease · 2026Article
- Schistosoma haematobium infection is associated with oncogenic gene expression in Cervical Mucosa, with enhanced effects following treatment: A pilot study.PLoS neglected tropical diseases · 2025Article
- HNF4A promotes tumor progression in gastric cancer by transcriptional activation of KIF2C.Clinical and experimental medicine · 2025Article
- Sex-Specific Concordance of Striatal Transcriptional Signatures of Opioid Addiction in Human and Rodent Brains.Biological psychiatry global open science · 2025Article
- Exploring the role of LOX family in glioma progression and immune modulation.Frontiers in immunology · 2025Article
- Unveiling the link between arsenic toxicity and diabetes: an in silico exploration into the role of transcription factors.Toxicological research · 2024Article
- Long non-coding RNA NEAT1 promotes aerobic glycolysis and progression of cervical cancer through WNT/β-catenin/PDK1 axis.Cancer medicine · 2024Article
- HNF4A-Bridging the Gap Between Intestinal Metaplasia and Gastric Cancer.Evolutionary bioinformatics online · 2024Article
- SNHG3/WISP2 Axis Promotes Hela Cell Migration and InvasionCancer genomics & proteomics · 2023Article
- Article
- The role of hepatocyte nuclear factor 4α (HNF4α) in tumorigenesis.Frontiers in oncology · 2022Review
- Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocyte nuclear factor 4 alpha (HNF4A) is a transcriptional factor which plays an important role in the development of the liver, kidney, and intestines. Nevertheless, its role in cervical cancer and the underlying mechanism remain unknown. In this study, both immunohistochemistry and western blotting revealed that the expression of HNF4A was downregulated in cervical cancer. Xenograft assays suggested that HN4A could inhibit tumorigenic potential of cervical cancer in vivo. Functional studies illustrated that HNF4A also inhibited the proliferation and viability of cervical cancer cells in vitro. In addition, FACS analysis implied that HNF4A could induce cell cycle arrest from the G0/G1 phase to S phase. Further studies suggested that HNF4A downregulated the activity of the Wnt/
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