小发夹RNA
小RNA
癌症研究
细胞生长
基因敲除
细胞凋亡
转移
异位表达
基因沉默
生物
医学
病理
癌症
细胞培养
内科学
基因
遗传学
生物化学
作者
Xin Ning,Guangyue Shi,Sujing Ren,Shuang Liu,Jing Ding,Ruichun Zhang,Lianwei Li,Qin Xie,Wei Xu,Fanling Meng,Rong Ma
出处
期刊:Oncologist
[Wiley]
日期:2022-01-01
卷期号:27 (1): e64-e75
被引量:6
标识
DOI:10.1093/oncolo/oyab015
摘要
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).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.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.The glioblastoma-amplified sequence may regulate the proliferation and metastasis of OC cells by combining with eEF1A1.
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