GSG2 Promotes Development and Predicts Poor Prognosis of Ovarian Cancer

Abstract

Purpose

Ovarian cancer is one of the most common malignant tumors in gynecology, whose treatment was seriously limited by the unclear understanding of molecular mechanism in disease development. GSG2, also known as Haspin, is a novel molecule found to be involved in human cancers.

Materials and Methods

In this study, immunohistochemical analysis was used to detect GSG2 expression in ovarian cancer tissues and corresponding normal tissues. Statistical analysis was performed to construct relationship between GSG2 and tumor characteristics as well as prognosis. Ovarian cell model with GSG2 knockdown was constructed through lentivirus-mediated transfection of shRNA, which was used in MTT assay, colony formation assay and flow cytometry for investigating the role of GSG2 in ovarian cancer. A human apoptosis antibody array was used to identify potential downstream apoptosis-related proteins of GSG2.

Results

The results demonstrated the upregulation of GSG2 in ovarian cancer, whose expression was positively related to tumor grade and AJCC stage, and negatively correlated with patients’ prognosis. Moreover, knockdown of GSG2 inhibited ovarian cancer development through suppressing cell growth and inducing cell apoptosis. Further exploration revealed that a variety of apoptosis-related and PI3K signaling pathway-related proteins may be implicated in the GSG2 induced regulation of ovarian cancer.

Conclusion

In summary, it was illustrated that GSG2 was involved in the development of ovarian cancer, which has the potential to become therapeutic target and prognostic indicator in ovarian cancer treatment.

Keywords:

• ovarian cancer
• GSG2
• prognosis
• cell proliferation
• cell apoptosis

Data Sharing Statement

Not applicable.

Ethics Approval and Informed Consent

This study was approved by Ethics committee of Fudan university. Informed consents were collected from all the patients in this study.

Consent for Publication

Not applicable.

Disclosure

The authors report no conflicts of interest for this work.