ArticleEpigenetics & chromatin2025
Acetylation modification of AIM2 by KAT2B suppresses the AKT/Wnt/β-catenin signaling pathway activation and inhibits breast cancer progression.
Article in Epigenetics & chromatin, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- MiR-494-5p suppresses colorectal cancer metastasis by multi-level targeting of KAT2B, a novel mechanism disrupting KAT2B enhancer-promoter looping, and inhibiting c-JUN-driven pro-metastatic properties.Molecular cancer · 2026Article
- Subtype-Stratified Consensus Gene Signatures: Bridging Tumor Cell Biology, Immune Microenvironment, and Clinical Prognosis in Breast Cancer.International journal of molecular sciences · 2026Article
- Wnt/β-Catenin-mTOR-autophagy crosstalk in breast cancer: context-dependent control of tumor progression, immune suppression, and therapeutic resistance.Frontiers in immunology · 2026Review
- Correction: Acetylation modification of AIM2 by KAT2B suppresses the AKT/Wnt/β-catenin signaling pathway activation and inhibits breast cancer progression.Epigenetics & chromatin · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors.
Funding
Abstract
backgroundThe development of breast cancer is known to be greatly influenced by epigenetic changes. The impact of histone acetyltransferase KAT2B on AIM2 and AKT/Wnt/β-catenin signaling have not been studied yet.
methodsIn this study, clinical breast cancer tissue and para-cancer tissue samples were collected from 60 breast cancer patients, and correlations between AIM2 expression and pathological parameters were analyzed. Breast cancer cell lines were obtained for in vitro studies, and AIM2 overexpression or KAT2B knockdown models were constructed. The CCK8 and Edu assay were conducted to measure cell proliferation, and cell invasion was determined by Transwell analysis. For mRNA and protein expression measurement, RT-qPCR and western blotting were utilized, respectively. Co-immunoprecipitation was used to investigate the interaction between KAT2B and AIM2. Animal models were established using BALB/c-nu mice through subcutaneous injection with breast cancer cells transfected with AIM2 K90R mutant vectors. Expression of Ki-67, KAT2B and AIM2 AcK90 was measured using immunohistochemistry.
resultsThe clinical samples showed that AIM2 was downregulated in breast cancer tissues and was linked to lymph node metastases and advanced clinical stage. Subsequently, the in vitro studies found that AIM2 exerted a suppressive impact on the growth, spread, and invasion of breast cancer cells. We further demonstrated that KAT2B mediates acetylation of AIM2 at the lysine 90 residue, which suppresses cancer cell growth, invasion, and migration through inhibiting the AKT/Wnt/β-catenin axis. In animal models, we further confirmed that acetylation of AIM2 inhibited the stimulation of the AKT/Wnt/β-catenin axis, thereby suppressing breast cancer growth in vivo. Finally, we proved that the KAT2B and acetylation of AIM2 correlated with the prognosis of clinical breast cancer.
conclusionOur study suggests that KAT2B-mediated acetylation of AIM2 can suppress the stimulation of the AKT/Wnt/β-catenin axis, consequently inhibiting breast carcinoma progression.
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