Effect of activation of the Akt/mTOR signaling pathway by EEF1A2 on the biological behavior of osteosarcoma.

Abstract

BACKGROUND:

Osteosarcoma (OS) is a common bone cancer in children and adolescents which causes a large number of cancer-related deaths. Eukaryotic Translation Elongation Factor 1 Alpha 2 (EEF1A2) has been revealed to have carcinogenic properties and promote tumor progression in many cancers. We want to investigate the biological function and mechanism of EEF1A2 in OS.

METHODS:

The expression of EEF1A2 in OS was investigated using the Gene Expression Omnibus (GEO) database and quantitative reverse transcription polymerase chain reaction (qRT-PCR). The biological function of EEF1A2 in OS was studied using cell counting kit-8 (CCK8) assay, 5-ethynyl-2'-deoxyuridine (EdU) assay, Transwell assay, and OS of xenograft nude mice model. Real-time fluorescence quantitative PCR was used to detect the expression level of EEF1A2 mRNA in OS tissues and cell lines. Western blot was used to detect the phosphorylation level of Akt and mTOR.

RESULTS:

There was high expression of EEF1A2 in OS, which was closely related to the Enneking stage and tumor size of OS. In vitro, EEF1A2 promoted the proliferation, migration, and invasion of OS cells; in vivo, EEF1A2 promoted the growth of OS tumors. The mechanism study showed that EEF1A2 can promote protein kinase B (Akt) and mammalian target of rapamycin (mTOR) phosphorylation, thereby activating the Akt/mTOR signaling pathway in OS.

CONCLUSION:

There is high expression of EEF1A2 in OS, which can promote the proliferation, migration, and invasion of OS cells in vitro and the growth of OS tumors in vivo via activation of the Akt/mTOR signaling pathway.

• Authors: Jianing Yang, Jun Tang, Juan Li, Ying Cen, Junjie Chen, Gengwu Dai
• Journal: Annals of translational medicine (Ann Transl Med) Vol. 9 Issue 2 Pg. 158 (Jan 2021) ISSN: 2305-5839 [Print] China
• PMID: 33569460 (Publication Type: Journal Article)
• Copyright: 2021 Annals of Translational Medicine. All rights reserved.