4.7 Article

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

Journal

ONCOLOGIST
Volume 27, Issue 1, Pages E64-E75

Publisher

OXFORD UNIV PRESS
DOI: 10.1093/oncolo/oyab015

Keywords

GBAS; ovarian cancer; prognosis; proliferation; metastasis

Categories

Funding

  1. Liande Wu Science Foundation for Young Scholars of Harbin Medical University Cancer Hospital [WLD-QN1705]
  2. Jingying Foundation of the Harbin Medical University Cancer Hospital [JY2015-04]
  3. Medical Award Foundation Project of Beijing [YXJL-2021-0577-0421]
  4. Science and Technology Innovation Medical Development Foundation Project of Beijing [KC2021-JF-0055-01]

Ask authors/readers for more resources

GBAS is a newly identified gene that is amplified in approximately 40% of glioblastomas. This article investigates the expression, prognostic significance, and possible pathways of GBAS in ovarian cancer. The study found that GBAS is overexpressed in ovarian cancer and is associated with lymph node metastasis. Inhibition of GBAS expression reduces cell proliferation and migration and promotes apoptosis in ovarian cancer cells. Further research suggests that GBAS may regulate cancer progression through mitochondria-associated pathways and can be targeted by specific microRNAs.
GBAS is a newly identified gene that is amplified in approximately 40% of glioblastomas. This article reports on the expression, prognostic significance, and possible pathways of GBAS in ovarian cancer. 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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.7
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available