NCAPH is upregulated in endometrial cancer and associated with poor clinicopathologic characteristics.

Abstract

Recently, NCAPH (non-SMC condensin I complex subunit H), a regulatory subunit of the condensin complex, has captured our attention in various cancer studies. However, the function of NCAPH in endometrial cancer (EC) remains unclear. Our study aims to investigate the role of NCAPH in EC. The expression of NCAPH in EC tissues and normal tissues was predicted by The Cancer Genome Atlas (TCGA). The Kaplan-Meier analysis was performed to evaluate the impact of NCAPH expression on EC patients' survival. Logistic regression was used to study the correlation of NCAPH expression with clinicopathologic characteristics. Molecular mechanisms behind NCAPH in EC were evaluated by Gene Set Enrichment Analysis, genetic mutations, copy number variation, and DNA methylation level. NCAPH was significantly upregulated in EC (p=1e-24), and its expression level was significantly related to the more advanced International Federation of Gynecology & Obstetrics (FIGO) stage (stage IV vs. stage I: odd ratio.[OR]=3.7), higher grade (poor vs. well & moderate: OR=5.3), serous histology subtype (SEA vs. EEA: OR=8.5), myometrial invasion (≥50vs.<50 invasion: OR=1.8), metastasis (vs. no metastasis: OR=2.5), and with-tumor status (vs. free of tumor: OR=2.3) (all p were less than .05). The Gene Set Enrichment Analysis method indicated that MITOTIC_SPINDLE, G2M_CHECKPOINT, MYC_TARGETS_V1, E2F_TARGETS, MYC_TARGETS_V2, and MTORC1_SIGNALING were involved in the upregulated NCAPH group. NCAPH hypomethylation, amplified copy number variations and genetic mutations; all played a contributive role in NCAPH upregulation. These results reveal NCAPH functions as oncogene and promote the development of EC.