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GSG2 促进卵巢癌的发展并预测其不良预后
Authors Huang Y, Liu Y, Zhu K, Ma X, Lu R, Zhang M
Received 30 July 2020
Accepted for publication 17 December 2020
Published 19 January 2021 Volume 2021:13 Pages 499—508
DOI https://doi.org/10.2147/CMAR.S274807
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 4
Editor who approved publication: Prof. Dr. Xueqiong Zhu
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