# Bioinformatics and experimental analysis revealed the cancer-promoting role of NCAPG2 in epithelial ovarian cancer

## TL;DR

This study shows that NCAPG2 promotes epithelial ovarian cancer and could be a new treatment target.

## Contribution

The study identifies NCAPG2 as a novel therapeutic target in epithelial ovarian cancer through bioinformatics and experimental validation.

## Key findings

- NCAPG2 is significantly overexpressed in epithelial ovarian cancer tissues and cells.
- Knockdown of NCAPG2 inhibits cancer cell proliferation, migration, and invasion via the EMT pathway.
- High NCAPG2 expression correlates with advanced clinical stages of epithelial ovarian cancer.

## Abstract

Ovarian cancer (OC) is one of the most common gynecological malignancies with an extremely poor prognosis. Among them, epithelial ovarian cancer (EOC) is the most common histological type and exhibits more aggressive behavior. Non-SMC condensin II complex subunit G2 (NCAPG2) is crucial for the execution of chromosomal mitosis and the promotion of tumorigenesis, but its role in the progression of EOC remains unclear.

In this study, we first analyzed the expression of NCAPG2 in EOC using data from the cancer genome atlas program (TCGA) database, Genotype-Tissue Expression (GTEx) project, and the Gene Expression Omnibus (GEO) dataset (GSE9891). Subsequently, bioinformatics tools were used to explore the expression of NCAPG2 in EOC and its related functions. In addition, we also evaluated the role of NCAPG2 in DNA damage repair, chemotherapy resistance, immune cell infiltration, and immunotherapy response. Finally, its expression and function have been verified through clinical samples and in vitro experiments.

Analyses of databases revealed that NCAPG2 is significantly overexpressed in EOC tissues and cells. NCAPG2 plays a role in DNA damage repair, chemotherapy resistance, immune cell infiltration, and immunotherapy response. More importantly, knockdown of NCAPG2 by siRNA can inhibit the proliferation, migration, and invasion abilities of EOC cells A2780 and OVCAR3 in vitro through the epithelial-mesenchymal transition (EMT) signaling pathway. Clinical specimens have confirmed that NCAPG2 is highly expressed in EOC tissues and is closely related to the clinical stage.

High expression of NCAPG2 can promote the progression of EOC and may serve as a potential novel therapeutic target for EOC.