MicroRNA‑1236‑3p inhibits human osteosarcoma growth
- Jiarui Li
- Junxin Chen
- Zhijun Hu
- Wenbin Xu
Affiliations: Department of Urology Surgery, The First Affiliated Hospital of Nanchang University, Medical College of Nanchang University, Nanchang, Jiangxi 330000, P.R. China, Department of Orthopedic Surgery, Sir Run Run Shaw Hospital, Medical College of Zhejiang University & Key Laboratory of Musculoskeletal System Degeneration and Regeneration Translational Research of Zhejiang Province, Hangzhou, Zhejiang 310016, P.R. China
- Published online on: October 15, 2020 https://doi.org/10.3892/ol.2020.12229
Copyright: © Li
et al. This is an open access article distributed under the
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Osteosarcoma (OS) is a common bone tumor with high mortality worldwide. The long‑term survival rate of patients with metastatic or recurrent disease is <20%. The present study explored the biological role of microRNA (miRNA/miR)‑1236‑3p in OS. miRNA and mRNA expression levels were measured via reverse transcription‑quantitative PCR. Fluorescence in situ hybridization was performed to determine miR‑1236‑3p expression levels in clinical specimens. Protein expression was measured via western blotting. Immunohistochemical analysis was used to detect Wnt target gene expression in tumor tissues. The interaction between the Wnt3a 3'untranslated region and miR‑1236‑3p was assessed via dual‑luciferase reporter assays. Cell cycle, Transwell, Cell Counting Kit‑8 and wound healing assays were conducted to evaluate the function of the miR‑1236‑3p/Wnt3a axis. Human OS (HOS) cells stably transfected with vector or miR‑1236‑3p sponge were injected subcutaneously into nude mice to assess the role of miR‑1236‑3p in vivo. miR‑1236‑3p expression was downregulated in OS tissues compared with chondroma tissues, and miR‑1236‑3p overexpression inhibited OS cell migration and proliferation compared with the negative control group. Furthermore, in vivo xenograft assays displayed enhanced tumour growth rates in the miR‑1236‑3p sponge group compared with the vector control group. In the present study, the results indicated that miR‑1236‑3p inhibited OS progression and Wnt3a was identified as a target of miR‑1236‑3p.