ArticleOncotarget2016
Loss of AIM2 expression promotes hepatocarcinoma progression through activation of mTOR-S6K1 pathway.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 2 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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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
84 citing papers in PubMed, 2 syntheses or guidelines pooled it, 129 citations in OpenAlex.
- Metabolic cell death in cancer: mechanisms and therapeutic potential.Apoptosis : an international journal on programmed cell death · 2025Pooled it
- Inflammasomes and their roles in the pathogenesis of viral hepatitis and their related complications: An updated systematic review.Immunology letters · 2019Pooled it
- Review
- Establishment and validation of a prognostic model for pancreatic cancer utilizing genes of tumor-associated neutrophils.Discover oncology · 2026Article
- Chemerin Promotes Oral Squamous Cell Carcinoma Progression via NLRP3-Mediated Pyroptosis and the GSDMD-N Pathway.International dental journal · 2026Article
- The pyroptosis and inflammatory response-related long noncoding RNA signature as a novel prognostic biomarker of head and neck squamous cell carcinoma.Discover oncology · 2026Article
- A Comprehensive Review of AIM2 in Cancer: Functional Roles, Molecular Pathways, and Clinical Relevance.Journal of immunology research · 2026Review
- Pyroptosis in cancer therapy: a double-edged sword for immune activation and tumor progression.Molecular cancer · 2025Review
- rs604702 confers breast cancer risk by influencing PCAT18/miR-759/SPRR3 axis.Discover oncology · 2025Article
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- 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
- Regulation of cancer by inflammasomes: from inflammation to tumorigenesis.Frontiers in immunology · 2025Review
- The Role of AIM2 in Cancer Development: Inflammasomes and Beyond.Journal of Cancer · 2025Review
- The Role of Inflammasome-Associated Innate Immune Receptors in Cancer.Immune network · 2024Review
- Hepatocellular carcinoma and AIM2: Therapeutic potential through regulation of autophagy and macrophage polarization.Immunity, inflammation and disease · 2024Article
- AIM2 enhances Candida albicans infection through promoting macrophage apoptosis via AKT signaling.Cellular and molecular life sciences : CMLS · 2024Article
- Cytosolic DNA sensor AIM2 promotes KRAS-driven lung cancer independent of inflammasomes.Cancer science · 2024Article
- New prospects of cancer therapy based on pyroptosis and pyroptosis inducers.Apoptosis : an international journal on programmed cell death · 2024Review
- AIM2 promotes irradiation resistance, migration ability and PD-L1 expression through STAT1/NF-κB activation in oral squamous cell carcinoma.Journal of translational medicine · 2024Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Absent in melanoma (AIM2) is a member of the interferon-inducible HIN-200 protein family and is recently recognized to play an important dual role in both innate immunity and tumor pathology. However, the role of AIM2 in the development of hepatocellular carcinoma (HCC) remains to be clarified. Here we showed that AIM2 expression was significantly decreased in liver cancer tissues, and loss of its expression was significantly correlated with more advanced tumor progression. Exogenous overexpression of AIM2 in HCC cells suppressed mammalian target of rapamycin (mTOR)-S6K1 pathway and further inhibited proliferation, colony formation and invasion of HCC cells. On the contrary, block of AIM2 in HCC cells induced (mTOR)-S6K1 pathway activation and thus promoted HCC progression. Treatment with mTOR pathway inhibitor rapamycin further verified its contribution to HCC progression in AIM2 absent HCC cells. Thus, these data suggested that AIM2 played a critical role as a tumor suppressor and might serve as a potential therapeutic target for future development of AIM2-based gene therapy for human liver cancer. This study also paves a new avenue to treat AIM2-deficient cancer by suppression of mTOR.
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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.