ArticleCancer management and research2019
The oncogenic role of GNL3 in the progression and metastasis of osteosarcoma.
Article in Cancer management and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
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- Gelatin-based biomaterials as a delivery strategy for osteosarcoma treatment.Frontiers in pharmacology · 2025Review
- Expression of E-cadherin and N-cadherin in Epithelial-to-Mesenchymal Transition of Osteosarcoma: A Systematic Review.Cureus · 2023Review
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- GNL3 Regulates SIRT1 Transcription and Promotes Hepatocellular Carcinoma Stem Cell-Like Features and Metastasis.Journal of oncology · 2022Article
- miRNA-451 regulates rhesus choroid-retinal endothelial cell function and proteome profile.International journal of ophthalmology · 2022Article
- Identification of Binding Proteins for TSC22D1 Family Proteins Using Mass Spectrometry.International journal of molecular sciences · 2021Article
- The lncRNA ALMS1-IT1 may promote malignant progression of lung adenocarcinoma via AVL9-mediated activation of the cyclin-dependent kinase pathway.FEBS open bio · 2021Article
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- Development and validation of a prediction model for lung adenocarcinoma based on RNA-binding protein.Annals of translational medicine · 2021Article
- HOPX Is an Epigenetically Inactivated Tumor Suppressor and Overexpression of HOPX Induce Apoptosis and Cell Cycle Arrest in Breast Cancer.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGNL3 has been reported to be up-regulated in cancers and function in tumor progression, whereas the role of GNL3 in the progression of osteosarcoma remains unclear. MATERIALS AND
methodsIn this study, we blocked the expression of GNL3 by siRNA interference in osteosarcoma cell lines MG63 and U20S. CCK8, colony formation, wound-healing, Transwell, flow cytometry, and Hoechst/PI staining assays were used to examine the effects of GNL3 knockdown on cell proliferation, migration, invasion and apoptosis in MG63 and U20S cells. The relative activity of MMP9 was detected using Gelatin zymography assay. Western blot was performed to detect the expression of related proteins.
resultsWe found that silencing of GNL3 reduced the growth, migration, and invasion abilities of MG63 and U20S cells. Moreover, silencing GNL3 triggered cell cycle arrest in MG63 and U20S cells, as well as promoted cell apoptosis. In addition, depletion of GNL3 was observed to reduce the activity of MMP9 and suppress the process of epithelial-mesenchymal transition (EMT) through up-regulation of E-cadherin and down-regulation of N-cadherin. Furthermore, we found that X-box-binding protein 1 (XBP1) could bind to GNL3 using dual-luciferase reporter assay, and XBP1 overexpression could restore the inhibitory effects on proliferation, invasion, and EMT in MG63 and U20S cells caused by GNL3 knockdown.
conclusionThese data suggest that GNL3 functions as an oncogene in the progression of osteosarcoma by regulation of EMT, and XBP1 is also involved in its mechanism.
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