ArticleInternational journal of clinical and experimental medicine2015
The molecular mechanism of breast cancer cell apoptosis induction by absent in melanoma (AIM2).
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 25 citations in OpenAlex.
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Acetylation modification of AIM2 by KAT2B suppresses the AKT/Wnt/β-catenin signaling pathway activation and inhibits breast cancer progression.Epigenetics & chromatin · 2025Article
- 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
- Inhibition of NLRP3 inflammasome contributes to paclitaxel efficacy in triple negative breast cancer treatment.Scientific reports · 2024Article
- A method to comprehensively identify germline SNVs, INDELs and CNVs from whole exome sequencing data of BRCA1/2 negative breast cancer patients.NAR genomics and bioinformatics · 2024Article
- Absent in melanoma 2 attenuates proliferation and migration and promotes apoptosis of human colorectal cancer cells by activating P38MAPK signaling pathway.Oncology research · 2023Article
- The roles of inflammasomes in cancer.Frontiers in immunology · 2023Review
- Advances in Cancer Diagnosis: Bio-Electrochemical and Biophysical Characterizations of Cancer Cells.Micromachines · 2022Review
- Article
- NLRC4, ASC and Caspase-1 Are Inflammasome Components that Are Mediated by P2YInternational journal of molecular sciences · 2020Article
- NLRP3 Inflammasome From Bench to Bedside: New Perspectives for Triple Negative Breast Cancer.Frontiers in oncology · 2020Review
- Article
- Diverging inflammasome signals in tumorigenesis and potential targeting.Nature reviews. Cancer · 2019Review
- Ribosomal DNA as DAMPs Signal for MCF7 Cancer Cells.Frontiers in oncology · 2019Article
- H1/pAIM2 nanoparticles exert anti-tumour effects that is associated with the inflammasome activation in renal carcinoma.Journal of cellular and molecular medicine · 2018Article
- The contrasting roles of inflammasomes in cancer.American journal of cancer research · 2018Review
- HBx-mediated decrease of AIM2 contributes to hepatocellular carcinoma metastasis.Molecular oncology · 2017Article
- AIM2 regulates viability and apoptosis in human colorectal cancer cells via the PI3K/Akt pathway.OncoTargets and therapy · 2017Article
- PLMET: A Novel Pseudolikelihood-Based EM Test for Homogeneity in Generalilzed Exponential Tilt Mixture Models.Journal of the American Statistical Association · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo determine the molecular mechanism by which absent in melanoma 2 (AIM2) induces breast cancer cell apoptosis.
methodsEstablish Tet-Off(TM) model system to induce AIM2 expression in great quantities, MCF-7 tTA-AIM2 cells were the experimental group; MCF-7 tTA-Luc cells were the control group. The expression and subcellular localization of AIM2 in breast cancer cell lines were determined via Western Blotting. AIM2 protein expression was determined after the addition of interferon-γ (102 U/ml). Flow cytometry was used to analyze the effects of AIM2 on the cell cycle. Apoptosis detection was performed by staining with Annexin V-FITC and propidium iodide. Apoptosis mechanism was detected via Western Blotting. The XTT assay was used to analyze the effects of AIM2 on cell growth.
resultThis experiment established Tet-Off guidance system. This system results which promotes AIM2 gene transcription and increased AIM2 protein expression. Four days after induction, AIM2 expression was detected. AIM2 expression increased with the number of days post-induction. AIM2 is present in cytoplasm and nuclei. Interferon-γ (102 U/ml) induced AIM2 protein expression and significantly increased AIM2 expression. AIM2 expression had no significant effect on the cell cycle, With the increase of Cdk2 expression induced by days were gradually increased, and Cdk4, Cyclin E expression was no significantly difference. AIM2 expression can significantly promote the apoptosis of breast cancer cells. Increased AIM2 expression can inhibit the expression of the anti-apoptotic protein Bcl-xL, increase the expression of the apoptosis proteins Bad and Bax, and activate caspases, resulting in cleavage of the DNA repair protein PARP. The XTT assay showed that AIM2 expression slows the rate of cell growth.
conclusionIn this breast cancer Tet-Off(TM) system, AIM2 was expressed in the cytoplasm and nucleus, stimulated the mitochondria to promote apoptosis, and influenced cell survival and proliferation.
Indexed as
Identifiers
26628957PMC4658846W2414797142What OpenQuestion holds
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.