Lentivirus‑induced knockdown of IARS2 expression inhibits the proliferation and promotes the apoptosis of human osteosarcoma cells

Liu,Qi; Lin,Feng

doi:10.3892/ol.2022.13382

Lentivirus‑induced knockdown of IARS2 expression inhibits the proliferation and promotes the apoptosis of human osteosarcoma cells

Authors:
- Qi Liu
- Feng Lin
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Affiliations: Department of Oncology, The Eighth People's Hospital of Shanghai, Shanghai 200235, P.R. China
Published online on: June 15, 2022 https://doi.org/10.3892/ol.2022.13382
Article Number: 262
Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Isoleucyl‑tRNA synthetase 2 (IARS2), distributed in mitochondria, is an IARS involved in protein synthesis. Notably, IARS2 has been reported to be associated with tumor progression; however, the relationship between osteosarcoma (OS) and IARS2 remains unclear. To investigate the role of IARS2 in human OS, the expression and relationship of IARS2 with survival were firstly analyzed using the Gene Expression Profiling Interactive Analysis 2 database. Subsequently, an IARS2‑short hairpin RNA lentiviral vector was established and used to infect the MNNG/HOS and U2OS cell lines. Reverse transcription‑quantitative PCR (RT‑qPCR) and western blotting were applied to determine the efficiency of IARS2 knockdown. The effects of IARS2 knockdown on cell proliferation, colony formation and apoptosis were evaluated by Celigo, MTT assays, colony formation assays and flow cytomeric analysis. In the present study, IARS2 tends to be high expressed in OS tissue and was associated with survival but this was not significant. The results of RT‑qPCR and western blotting showed that the expression of IARS2 was effectively knocked down in the MNNG/HOS and U2OS cell lines. Celigo, MTT and colony formation assays showed that IARS2 knockdown in MNNG/HOS and U2OS cell lines inhibited cell proliferation and colony formation compared with in the control group. Flow cytometric analysis revealed that IARS2 knockdown increased apoptosis. These results suggested that IARS2 may be critical for the proliferation and apoptosis of OS cells.

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