ArticleCancer science2012
Overexpression of the DNA sensor proteins, absent in melanoma 2 and interferon-inducible 16, contributes to tumorigenesis of oral squamous cell carcinoma with p53 inactivation.
Article in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 83 citations in OpenAlex.
- Advancements and Clinical Applications Prospects of Epigenetic Biomarkers in Liquid Biopsy for Oral Squamous Cell Carcinoma.Current issues in molecular biology · 2026Review
- The Role of Inflammasomes in Chronic Oral Inflammatory Disease and Oral Cancer: A Narrative Review.Dentistry journal · 2025Review
- The immune-related prognostic gene AIM2 promotes pancreatic cancer progression via inflammasome.Scientific reports · 2025Article
- Role of the AIM2 Inflammasome in Cancer: Potential Therapeutic Strategies.Biomedicines · 2025Review
- The dual roles of human PYHIN family proteins in cancer: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- The Role of AIM2 in Cancer Development: Inflammasomes and Beyond.Journal of Cancer · 2025Review
- IFI16 promotes the progression of clear cell renal cell carcinoma through the IL6/PI3K/AKT axis.Journal of translational medicine · 2024Article
- Epigenetic Regulation in Oral Squamous Cell Carcinoma Microenvironment: A Comprehensive Review.Cancers · 2023Review
- System analysis based on the pyroptosis-related genes identifes GSDMD as a novel therapy target for skin cutaneous melanoma.Journal of translational medicine · 2023Article
- Cell-Free DNA in the Pathogenesis and Therapy of Non-Infectious Inflammations and Tumors.Biomedicines · 2022Review
- A pyroptosis-associated signature plays a role in prognosis prediction in clear cell renal cell carcinoma.BMC medical genomics · 2022Article
- Context-dependent functions of pattern recognition receptors in cancer.Nature reviews. Cancer · 2022Review
- A study on DNA methylation modifying natural compounds identified EGCG for induction of IFI16 gene expression related to the innate immune response in cancer cells.Oncology letters · 2022Article
- AIM2 inhibits the proliferation, invasion and migration, and promotes the apoptosis of osteosarcoma cells by inactivating the PI3K/AKT/mTOR signaling pathway.Molecular medicine reports · 2022Article
- Identification of a Novel Pyroptosis-Related Gene Signature Indicative of Disease Prognosis and Treatment Response in Skin Cutaneous Melanoma.International journal of general medicine · 2022Article
- AIM2 Promotes Gastric Cancer Cell Proliferation via the MAPK Signaling Pathway.Journal of healthcare engineering · 2022Article
- Comprehensive analysis identifies IFI16 as a novel signature associated with overall survival and immune infiltration of skin cutaneous melanoma.Cancer cell international · 2021Article
- Article
- The complex role of AIM2 in autoimmune diseases and cancers.Immunity, inflammation and disease · 2021Review
- Increased expression of IFI16 predicts adverse prognosis in multiple myeloma.The pharmacogenomics journal · 2021Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of oral squamous cell carcinoma (OSCC) is a multistep process that requires the accumulation of genetic alterations. To identify genes responsible for OSCC development, we performed high-density single nucleotide polymorphism array analysis and genome-wide gene expression profiling on OSCC tumors. These analyses indicated that the absent in melanoma 2 (AIM2) gene and the interferon-inducible gene 16 (IFI16) mapped to the hematopoietic interferon-inducible nuclear proteins. The 200-amino-acid repeat gene cluster in the amplified region of chromosome 1q23 is overexpressed in OSCC. Both AIM2 and IFI16 are cytoplasmic double-stranded DNA sensors for innate immunity and act as tumor suppressors in several human cancers. Knockdown of AIM2 or IFI16 in OSCC cells results in the suppression of cell growth and apoptosis, accompanied by the downregulation of nuclear factor kappa-light-chain-enhancer of activated B cells activation. Because all OSCC cell lines have reduced p53 activity, wild-type p53 was introduced in p53-deficient OSCC cells. The expression of wild-type p53 suppressed cell growth and induced apoptosis via suppression of nuclear factor kappa-light-chain-enhancer of activated B cells activity. Finally, the co-expression of AIM2 and IFI16 significantly enhanced cell growth in p53-deficient cells; in contrast, the expression of AIM2 and/or IFI16 in cells bearing wild-type p53 suppressed cell growth. Moreover, AIM2 and IFI16 synergistically enhanced nuclear factor kappa-light-chain-enhancer of activated B cells signaling in p53-deficient cells. Thus, expression of AIM2 and IFI16 may have oncogenic activities in the OSCC cells that have inactivated the p53 system.
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