1. Overexpression Pattern of miR-301b in Osteosarcoma and Its Relevance with Osteosarcoma Cellular Behaviors via Modulating SNX10.
- Author
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Wang Y, Sun N, Zhang Z, Zhou Y, Liu H, Zhou X, Zhang Y, and Zhao Y
- Subjects
- Humans, Cell Movement, Cell Line, Tumor, Cell Proliferation, Gene Expression Regulation, Neoplastic, Sorting Nexins genetics, Sorting Nexins metabolism, Bone Neoplasms genetics, Bone Neoplasms metabolism, Bone Neoplasms pathology, MicroRNAs, Osteosarcoma genetics, Osteosarcoma metabolism, Osteosarcoma pathology
- Abstract
Prior studies have noted the importance of microRNAs (miRNAs) in development and progression of osteosarcoma (OS), but the influence of miR-301b is less investigated. This investigation aimed to explore the biological role of miR-301b/SNX10 in OS. GSE28423 and GSE28424 arrays delivered the corresponding miR-301b and sorting nexin 10 (SNX10) expression levels in OS samples. miR-301b and SNX10 expressions were also measured by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting in cells. Cell counting kit (CCK)-8 and transwell analysis were applied to measure cell characteristics. Luciferase reporter assay and Pearson correlation analysis were used to detect the relevance between miR-301b and SNX10. miR-301b was extremely increased in OS tissues compared with normal tissues, while SNX10 was decreased. The proliferation, invasion, and migration capabilities were limited following a low expression level of miR-301b whereas miR-301b overexpression promoted cellular malignant behaviors. miR-301b negatively targeted SNX10. The elevated SNX10 expression highlighted the inhibitory function on cell proliferation, migration, and invasion in OS cells treated by miR-301b inhibitor. Reduction of miR-301b induced the decrease of epithelial-mesenchymal transition (EMT)-related markers including N-cadherin, Vimentin, and matrix metallo-proteinase 9 (MMP)9. These results are added to the complete expanding field of the potential effects of miR-301b in OS cell malignant behaviors and demonstrate its promising role for further use to treat human OS., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)
- Published
- 2023
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