ArticleInternational journal of oral science2022
FAM64A promotes HNSCC tumorigenesis by mediating transcriptional autoregulation of FOXM1.
Article in International journal of oral science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- The Regulatory Network of FOXM1: Orchestrating Cancer Progression and Resistance to Therapy.International journal of molecular sciences · 2026Review
- OCIAD2 Stabilizes Integrin β1 Signaling Through SNX17-Mediated Endosomal Recycling to Lipid Rafts and Modulates Cisplatin Response in HNSCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- FAM64A Potentiates Bladder Carcinoma Tumorigenesis and Metastasis Through PI3K/mTORC2/AKT Pathway Activation.Cancers · 2026Article
- Targeting FAM64A: a promising strategy to halt liver cancer angiogenesis and enhance immunity.American journal of cancer research · 2026Article
- Impact of HMGA1 on tumorigenesis, prognosis and immune microenvironment in HNSCC: a multi-omics study.NPJ precision oncology · 2025Article
- The complex role and molecular mechanism of family with sequence similarity genes in cancer: a comprehensive review.Discover oncology · 2025Review
- FAM64A regulates the malignant phenotype and tumor microenvironment of non-small cell lung cancer by activating the JAK/STAT3/PDL1 axis.Journal of molecular histology · 2025Article
- New frontiers in salivary extracellular vesicles: transforming diagnostics, monitoring, and therapeutics in oral and systemic diseases.Journal of nanobiotechnology · 2024Review
- ACTN1 promotes HNSCC tumorigenesis and cisplatin resistance by enhancing MYH9-dependent degradation of GSK-3β and integrin β1-mediated phosphorylation of FAK.Journal of experimental & clinical cancer research : CR · 2023Article
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- Targeting Squalene Epoxidase Confers Metabolic Vulnerability and Overcomes Chemoresistance in HNSCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- ATHENA: an independently validated autophagy-related epigenetic prognostic prediction model of head and neck squamous cell carcinoma.Clinical epigenetics · 2023Article
- RNF112-mediated FOXM1 ubiquitination suppresses the proliferation and invasion of gastric cancer.JCI insight · 2023Article
- Complex interaction and heterogeneity among cancer stem cells in head and neck squamous cell carcinoma revealed by single-cell sequencing.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Head and neck squamous cell carcinoma (HNSCC) still lacks effective targeted treatment. Therefore, exploring novel and robust molecular targets is critical for improving the clinical outcome of HNSCC. Here, we reported that the expression levels of family with sequence similarity 64, member A (FAM64A) were significantly higher in HNSCC tissues and cell lines. In addition, FAM64A overexpression was found to be strongly associated with an unfavorable prognosis of HNSCC. Both in vitro and in vivo evidence showed that FAM64A depletion suppressed the malignant activities of HNSCC cells, and vice versa. Moreover, we found that the FAM64A level was progressively increased from normal to dysplastic to cancerous tissues in a carcinogenic 4-nitroquinoline-1-oxide mouse model. Mechanistically, a physical interaction was found between FAM64A and forkhead box protein M1 (FOXM1) in HNSCC cells. FAM64A promoted HNSCC tumorigenesis not only by enhancing the transcriptional activity of FOXM1, but also, more importantly, by modulating FOXM1 expression via the autoregulation loop. Furthermore, a positive correlation between FAM64A and FOXM1 was found in multiple independent cohorts. Taken together, our findings reveal a previously unknown mechanism behind the activation of FOXM1 in HNSCC, and FAM64A might be a promising molecular therapeutic target for treating HNSCC.
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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.