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MiR-92a modulates proliferation, apoptosis, migration, and invasion of osteosarcoma cell lines by targeting Dickkopf-related protein 3.

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机构： [1]Orthopedic Department, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yanchang Road, Shanghai 200072, China. [2]Spinal Pain Research Institute, Tongji University School of Medicine, 301 Yanchang Road, Shanghai 200072, China. [3]Department of Laboratory Medicine, Shanghai Children's Medical Center, School of Medicine, Shanghai Jiaotong University, Shanghai, China [4]Department of Clinical Laboratory, Shanghai Fourth People's Hospital, Tongji University School of Medicine, 1878 North Sichuan Road, Shanghai, 200081, China.

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关键词： MiR-92a Osteosarcoma Proliferation Apoptosis DKK3

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Osteosarcoma (OS) is recognized as a common malignant tumor with a high trend of metastasis and diffusion. Despite the progresses that have been made in surgery, chemotherapy, and radiotherapy in the recent decades, the prognosis of patients with OS still remains poor. MiRNAs are being increasingly considered as new therapeutic targets for OS treatment. Our research aims to investigate the regulatory impact of miR-92a in the development of OS. Quantitative real-time PCR (qRT-PCR) results revealed that the expression of miR-92a was aberrantly overexpressed in human OS cell lines. By using cell counting kit-8 (CCK-8) assays, colony formation assays, flow cytometric analyses and Transwell assays, our data suggested that up-regulation of miR-92a promoted the proliferation, migration, and invasion of MNNG and U2OS cells, while inhibiting their apoptosis. In contrast, the knockdown of miR-92a effectively reversed these cellular biological behaviors. Furthermore, bioinformatics analysis indicated that Dickkopf-related protein 3 (DKK3) was a possible target of miR-92a. Subsequently, negative regulation of miR-92a on DKK3 was observed, which further supported the direct binding between them. In addition, silencing DKK3 rescued the inhibitory effect of miR-92a inhibitor on the development of OS. To sum up, our study revealed that miR-92a played a carcinogenic role in the growth of OS by promoting the tumorigenesis of OS cells via targeting of DKK3, thus revealing a new therapeutic target for OS. © 2019 The Author(s).

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出版当年[2019]版：

大类 | 4 区生物学

小类 | 4 区生化与分子生物学 4 区细胞生物学

最新[2023]版：

大类 | 3 区生物学

小类 | 3 区生化与分子生物学 4 区细胞生物学

第一作者：

第一作者机构： [1]Orthopedic Department, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yanchang Road, Shanghai 200072, China. [2]Spinal Pain Research Institute, Tongji University School of Medicine, 301 Yanchang Road, Shanghai 200072, China.

通讯作者：

通讯机构： [1]Orthopedic Department, Shanghai Tenth People's Hospital, Tongji University School of Medicine, 301 Yanchang Road, Shanghai 200072, China. [2]Spinal Pain Research Institute, Tongji University School of Medicine, 301 Yanchang Road, Shanghai 200072, China.

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