ArticleScientific reports2025
KAT2B inhibits proliferation and invasion via inactivating TGF-β/Smad3 pathway-medicated autophagy and EMT in epithelial ovarian cancer.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 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
- Autophagy in cancer-associated fibroblasts: its role in gastrointestinal cancers.Molecular cancer · 2026Review
- Evaluation of the Expression of Small Extracellular Vesicle Markers and Their Cargo in Treatment-Naïve Retinoblastoma Tumor Tissues.Translational vision science & technology · 2026Article
- Tumor Exosomal L1 Cell Adhesion Molecule Promotes Brain Metastasis of Lung Cancer.Research (Washington, D.C.) · 2026Article
- Molecular mechanisms underlying the inhibition of cell migration and invasion in endometriosis: Advances in pharmacological research (Review).Biomedical reports · 2025Review
- Tumor-specific MHC-II guides anthracycline exemption and immunotherapy benefit in breast cancer.Biomarker research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Lysine acetyltransferase 2B (KAT2B) plays a crucial role in epigenetic regulation and tumor pathogenesis. Our study investigates KAT2B's function in epithelial ovarian cancer (EOC) using in vivo and in vitro methods. Immunohistochemistry showed the KAT2B expression in EOC tissues. RNA sequencing (RNA-seq) further identified altered gene expression profiles following KAT2B silencing in EOC cells. Western blot and qRT-PCR were employed to assess the protein and mRNA expression, respectively. KAT2B downregulated in EOC tissues and correlated with both FIGO stage and grade. KAT2B silencing induced autophagy, enhancing cell proliferation and invasion, while overexpression had opposite effects. In vivo, KAT2B silencing increased tumor volume and weight, mitigated by autophagy inhibitor chloroquine. Bioinformatics and co-immunoprecipitation assays identified a KAT2B-SMAD7 interaction. Mechanistic investigations suggested that KAT2B knockdown enhanced autophagy via activation of the TGF-β/Smad3/7 signaling pathway, thereby driving epithelial-mesenchymal transition (EMT), proliferation, and invasion in EOC. Additionally, our data hint at a potential role for the AKT/mTOR pathway. KAT2B acts as a putative tumor suppressor in EOC, where its reduced expression correlates with advanced disease stages. It is implicated in the regulation of autophagy, proliferation, and invasion via the TGF-β/Smad3/7 pathway, positioning KAT2B as a candidate therapeutic target for EOC interventions.
Indexed as
Identifiers
What 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.