Non-SMC Condensin I Complex Subunit G Promotes the Proliferation, Invasion and Homologous Recombination Repair of Endometrial Cancer Through PI3K/AKT Signaling Pathway

Abstract

This study aimed to investigate the role of Non-SMC condensin I complex subunit G (NCAPG) in endometrial cancer (EC) progression and prognosis. The researchers utilized various techniques, including analysis of The Cancer Genome Atlas (TCGA) database, immunohistochemistry, qRT-PCR, Western blotting, and functional assays to assess the impact of NCAPG on EC cells. The TCGA analysis revealed that NCAPG was significantly associated with overall survival and disease-free survival in EC patients. Immunohistochemistry analysis further confirmed a positive correlation between NCAPG expression, histological grade, and myometrial invasion in EC tissues. In vitro experiments demonstrated that NCAPG promoted EC cell proliferation, invasion, and influenced the G1/S cell cycle transition. Additionally, NCAPG was found to regulate the expression of FANCD2 and RAD51 in the homologous recombination repair pathway, and its knockdown sensitized EC cells to poly (ADP-ribose) polymerase inhibitors. The study also revealed the involvement of the PI3K/AKT signaling pathway in mediating the effects of NCAPG on EC cells’ proliferation, invasion, and homologous recombination repair. In conclusion, NCAPG acts as an oncogene in EC, driving proliferation, invasion, and homologous recombination repair through the PI3K/AKT pathway. NCAPG expression correlates with EC prognosis, revealing its significance as a therapeutic target for advanced cases, illuminating EC progression mechanisms.