GINS2 Promotes Osteosarcoma Tumorigenesis via STAT3/MYC Axis

Author:

Ren Bingkai1ORCID,Zheng Yibin12ORCID,Nie Lizhong1ORCID,Wu Fanhui1ORCID,Huang Leiwen1ORCID,Wei Jingdu1ORCID,Yang Dong1ORCID

Affiliation:

1. Department of Orthopedics, The First Affiliated Hospital of Nanchang University, Nanchang, China

2. Department of Orthopedics, The Yiwu Central Hospital, Jinhua, Zhejiang, China

Abstract

GINS2 is overexpressed in several cancers, but little is known about its role in osteosarcoma (OS). A series of in vivo and in vitro experiments were conducted to explore the role of GINS2 in OS. In this study, we demonstrated that GINS2 was found to be highly expressed in OS tissues and cell lines, which was associated with poor outcomes in OS patients. GINS2 knockdown hindered the growth and induced apoptosis in OS cell lines in vitro. Furthermore, GINS2 knockdown effectively inhibited the growth of a xenograft tumor in vivo. By using an Affymetrix gene chip and intelligent pathway analysis, it was demonstrated that the GINS2 knockdown could reduce the expression of several targeted genes and reduce the activity of the MYC signaling pathway. Mechanically, LC-MS, CoIP, and rescue experiments revealed that GINS2 promoted tumor progression through the STAT3/MYC axis in the OS. Moreover, GINS2 was associated with tumor immunity and may be a potential immunotherapeutic target for OS.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Oncology

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