NCAPG promotes the progression of endometrial cancer (EC) through PI3K-AKT pathway and has potential as a novel tumor marker. However, the precise regulatory mechanism of NCAPG remains inadequately understood. In this study, we applied Assay for Transposase Accessible Chromatin with high-throughput sequencing (ATAC-Seq) analysis combined with chromatin immunoprecipitation-qPCR (CHIP) and Co-Immunoprecipitation (CoIP) analysis to analysis for the first time that NCAPG promotes EC cell proliferation, migration and invasion by affecting the binding of LEF1 to chromatin, thereby affecting the transcription of downstream SEMA7A. Mechanistically, SEMA7A regulated the PI3K-AKT signaling pathway by binding to the PI3K regulatory subunit p85, exerting its biological function. The NCAPG/LEF1/SEMA7A axis promoted EC tumorigenesis and progression by activating the PI3K-AKT signaling pathway. Additionally, LEF1 and SEMA7A were associated with the FIGO stage, pathological grade, and myometrial invasion in EC patients. The expressions of NCAPG, LEF1, and SEMA7A were highly consistent. Targeting this cascade may provide effective antitumor strategies to delay the progression of EC.
Keywords: LEF1; NCAPG; PI3K/AKT signaling pathway; SEMA7A; endometrioid carcinoma.
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