ArticleChinese medical journal2026
APC loss promotes endometrial cancer progression by upregulating FGF12 expression: An integrated multi-omics analysis.
Article in Chinese medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundEndometrial cancer (EC) is one of the most common gynecological cancers worldwide. High-order chromatin structure plays a critical role in regulating gene expression. Our previous study identified frequent mutations in the chromatin remodeling-related gene adenomatous polyposis coli ( APC ) in EC. Here, we investigated the role of APC in chromatin remodeling and EC progression.
methodsThe efforts of APC against EC cells in vitro and in vivo were characterized by g ene expression and overall survival analysis with The Cancer Genome Atlas (TCGA) database, Western blotting, RNA isolation and quantitative real-time polymerase chain reaction (RT-PCR), the integrated multiomics analysis, lentivirus transfection, nude mice tumorigenesis experiment, and immunohistochemistry.
resultsAPC expression was reduced in EC tissues, and APC -knockdown KLE cells exhibited enhanced cell migration. Integrated multi-omics analyses, including RNA sequencing (RNA-seq), assay for transposase-accessible chromatin by high-throughput sequencing (ATAC-seq), and high-through chromosome conformation capture (Hi-C), compared control and APC -knockdown KLE cells. These analyses identified fibroblast growth factor 12 ( FGF12 ) as a differentially expressed gene (DEG) localized to switched chromatin compartments, cell-specific boundaries, and loops, with elevated expression in APC -knockdown cells. High FGF12 expression correlated with poor prognosis in EC patients. Knockdown of FGF12 in APC -deficient KLE cells reversed the enhanced migratory phenotype.
conclusionsLoss of APC promotes EC cell migration and reprograms chromatin architecture to upregulate FGF12 , activating tumorigenesis-related protein kinase B (AKT) and mitogen-activated protein kinase (MAPK) signaling pathways and driving EC progression. Elevated FGF12 levels are associated with poor prognosis, highlighting its potential as a therapeutic target for EC patients with low APC expression.
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