Inhibition of NCAPG expression inactivates the Wnt/beta-catenin signal to suppresses endometrial cancer cell growth in vitro

Endometrial cancer (EC) ranks as the most prevalent malignancy occurring in the female genital tract. Non-SMC condensin I complex subunit G (NCAPG), a mitotic associated chromosomal condensing protein, is reported to be frequently abnormally expressed in several tumors and plays a vital role in carcinogenesis. Our study aimed to explore the effect of NCAPG on cell proliferation and apoptosis in EC cells and to determine the underlying mechanism. Expression and survival data of NCAPG in EC tissues were analyzed by bioinformatics methods. Cell proliferation was evaluated by EdU and CCK-8 assays. Apoptosis was assessed by flow cytometry analysis. Expression of NCAPG, proliferating cell nuclear antigen (PCNA), Ki67, Bcl-2, Bax, active caspase-3, active beta-catenin, and c-Myc were determined by western blotting. NCAPG was highly expressed in EC tissues and cells and predicted poor survival for EC patients. NCAPG knockdown inhibited cell proliferation and induced apoptosis in EC cells. Additionally, NCAPG knockdown inactivated the Wnt/beta-catenin pathway in EC cells. Mechanistically, beta-catenin overexpression blocked the tumorigenic effects of NCAPG in EC cells. In conclusion, NCAPG silencing inhibited cell proliferation and induced apoptosis in EC cells via inhibiting the Wnt/beta-catenin pathway.

Automated summary

The study revealed that NCAPG is highly expressed in EC tissues and cells, and its knockdown inhibits cell proliferation and induces apoptosis in EC cells by suppressing the Wnt/beta-catenin pathway.