ArticleThe oncologist2022
GBAS Regulates the Proliferation and Metastasis of Ovarian Cancer Cells by Combining with eEF1A1.
Article in The oncologist, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- UCHL3 promotes hepatocellular carcinoma progression by stabilizing EEF1A1 through deubiquitination.Biology direct · 2024Article
- Atherosclerosis-related biomarker PABPC1 predicts pan-cancer events.Stroke and vascular neurology · 2024Article
- Immune cell infiltration and drug response in glioblastoma multiforme: insights from oxidative stress-related genes.Cancer cell international · 2024Article
- TRIM47 promotes ovarian cancer cell proliferation, migration, and invasion by activating STAT3 signaling.Clinics (Sao Paulo, Brazil) · 2022Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe 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).
methodImmunohistochemical 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.
resultsImmunohistochemistry 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.
conclusionThe glioblastoma-amplified sequence may regulate the proliferation and metastasis of OC cells by combining with eEF1A1.
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