GBAS Regulates the Proliferation and Metastasis of Ovarian Cancer Cells by Combining with eEF1A1

Author:

Ning Xin1,Shi Guangyue2,Ren Sujing1,Liu Shuang1,Ding Jing1,Zhang Ruichun1,Li Lianwei1,Xie Qin1,Xu Wei1,Meng Fanling1ORCID,Ma Rong1

Affiliation:

1. Department of Gynecology, Harbin Medical University Cancer Hospital, Harbin, People’s Republic of China

2. Department of Oncology, Harbin Medical University Cancer Hospital, Harbin, People’s Republic of China

Abstract

Abstract Background The glioblastoma-amplified sequence (GBAS) is a newly identified gene that is amplified in approximately 40% of glioblastomas. This article probes into the expression, prognostic significance, and possible pathways of GBAS in ovarian cancer (OC). Method Immunohistochemical methods were used to evaluate the expression level of GBAS in OC and its relationship with clinicopathological characteristics and prognosis. Glioblastoma-amplified sequence shRNA was designed to transfect into OC cell lines to silence GBAS expression, then detect the proliferation, apoptosis, and migration ability of the cell. Furthermore, an in vitro tumor formation experiment in mice was constructed to prove the effect of GBAS expression on the growth of OC in vivo. To further study the regulation mechanism of GBAS, we performed co-immunoprecipitation (Co-IP) and shotgun LC-MS mass spectrometry identification. Results Immunohistochemistry indicated that GBAS was markedly overexpressed in OC compared with normal ovarian tissue and was associated with lymph node metastasis. Inhibition of GBAS expression can significantly reduce OC cell proliferation, colony formation, promote cell apoptosis, and reduce the ability of cell migration and invasion. In vivo tumor formation experiments showed that the size and weight of tumors in mice after GBAS expression knockdown was significantly smaller. Glioblastoma-amplified sequence may be combined with elongation factor 1 alpha 1 (eEF1A1) to achieve its regulation in OC. Bioinformatics analysis data indicate that GBAS may be a key regulator of mitochondria-associated pathways, therefore controlling cancer progression. MicroRNA-27b, MicroRNA-23a, and MicroRNA-590 may directly targeting GBAS affects the biological behavior of OC cells. Conclusion The glioblastoma-amplified sequence may regulate the proliferation and metastasis of OC cells by combining with eEF1A1.

Funder

Harbin Medical University Cancer Hospital

The Medical Award Foundation Project of Beijing

The Science and Technology Innovation Medical Development Foundation Project of Beijing

Publisher

Oxford University Press (OUP)

Subject

Cancer Research,Oncology

Reference41 articles.

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