ArticleCarcinogenesis2018
AFF4 promotes tumorigenesis and tumor-initiation capacity of head and neck squamous cell carcinoma cells by regulating SOX2.
Article in Carcinogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- FENDRR represses Bladder Cancer Cell Proliferation, Stemness, Migration, Invasion, and EMT Process by Targeting miR-18a-5p/AFF4 Axis.Biochemical genetics · 2025Article
- Disease-linked regulatory DNA variants and homeostatic transcription factors in epidermis.Nature communications · 2025Article
- AFF4 promotes tumor progression and cisplatin resistance by modulating the PTEN/PI3K/AKT/mTOR axis to accelerate glycolysis in lung adenocarcinoma.Cell & bioscience · 2025Article
- The Biological Significance of AFF4: Promoting Transcription Elongation, Osteogenic Differentiation and Tumor Progression.Combinatorial chemistry & high throughput screening · 2024Review
- Novel perspectives on autophagy-oxidative stress-inflammation axis in the orchestration of adipogenesis.Frontiers in endocrinology · 2024Review
- Multiple Genomic Alterations, Including a NovelInternational journal of molecular sciences · 2023Review
- Gene signature of m6A-related targets to predict prognosis and immunotherapy response in ovarian cancer.Journal of cancer research and clinical oncology · 2023Article
- PI3K/ c-Myc/AFF4 axis promotes pancreatic tumorigenesis through fueling nucleotide metabolism.International journal of biological sciences · 2023Article
- AFF4 regulates cellular adipogenic differentiation via targeting autophagy.PLoS genetics · 2022Article
- Butylidenephthalide Abrogates the Snail-Induced Cancer Stemness in Oral Carcinomas.International journal of molecular sciences · 2022Article
- AFF4 Predicts the Prognosis of Colorectal Cancer Patients and Suppresses Colorectal Cancer MetastasisFrontiers in oncology · 2022Article
- MiR-425-5p accelerated the proliferation, migration, and invasion of ovarian cancer cells via targeting AFF4.Journal of ovarian research · 2021Article
- Identification of Common Driver Gene Modules and Associations between Cancers through Integrated Network Analysis.Global challenges (Hoboken, NJ) · 2021Article
- Therapeutic targeting of transcriptional elongation in diffuse intrinsic pontine glioma.Neuro-oncology · 2021Article
- Blocking the GITR-GITRL pathway to overcome resistance to therapy in sarcomatoid malignant pleural mesothelioma.Communications biology · 2021Article
- The Expression and Roles of the Super Elongation Complex in Mouse Cochlear Lgr5+ Progenitor Cells.Frontiers in cellular neuroscience · 2021Article
- HPVTranslational oncology · 2021Review
- AFF4 regulates osteogenic differentiation of human dental follicle cells.International journal of oral science · 2020Article
- The mStem cells international · 2020Article
- Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Super elongation complex (SEC) controls gene transcription by releasing Pol II from pausing. Previous studies have shown that dysfunction of SEC was associated with multiple human cancers, such as leukemia and breast cancer. However, the role of SEC in head and neck squamous cell carcinoma (HNSCC) development remains largely unknown. In this study, we found expression of AF4/FMR2 family member 4 (AFF4), the core component of SEC, was upregulated dramatically in HNSCC cell lines and tumor tissues. By using siRNA-mediated depletion and overexpression of AFF4, we demonstrated AFF4 promoted proliferation, migration and invasion of HNSCC cells. Moreover, we found AFF4 enhanced the aldehyde dehydrogenase (ALDH) activity and sphere formatting activity and was required for the tumor-initiation capacity of stem-like cells in HNSCC cell lines. Mechanistically, we found the role of AFF4 in regulation of HNSCC cell behaviors was mainly mediated by sex-determining region Y box2 (SOX2), a critical regulator involved in development of several human cancers. SOX2 expression changed in parallel with AFF4 expression in response to depletion and overexpression of AFF4, respectively. More importantly, overexpression of SOX2 rescued the inhibited proliferation, migration, invasion and ALDH activity induced by knockdown of AFF4 in HNSCC cells, at least in part. Collectively, our findings indicate AFF4 may serve as a biomarker and a potential target of therapies for patients with HNSCC.
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