期刊
AGING-US
卷 13, 期 16, 页码 20116-20130出版社
IMPACT JOURNALS LLC
关键词
RUSC1-AS1; miR-340-5p; PI3K/AKT; osteosarcoma
资金
- Science and Technology Plan of Nanshan District of Shenzhen City, China [2020113]
- Young Talents' Science and Technology Innovation Project of Hainan Association for Science and Technology [QCXM202018]
The upregulation of lncRNA RUSC1-AS1 in osteosarcoma promotes cell proliferation, invasion, and inhibits apoptosis, as well as enhances the epithelial-mesenchymal transition (EMT) process. Inhibition of RUSC1-AS1 also showed suppressive effects on tumor growth in vivo, indicating its potential as a therapeutic target for osteosarcoma.
Dysregulation of long noncoding RNA (lncRNA) is frequently involved in the progression and development of osteosarcoma. LncRNA RUSC1-AS1 is reported to be upregulated and acts as an oncogene in hepatocellular carcinoma, cervical cancer and breast cancer. However, its role in osteosarcoma has not been studied yet. In the present study, we investigated the role of RUSC1-AS1 in osteosarcoma both in vitro and in vivo. The results showed that the expression of RUSC1-AS1 was significantly upregulated in osteosarcoma cell line U2OS and HOS compared to that in human osteoblast cell line hFOB1.19. Similar results were found in human samples. Silencing RUSC1-AS1 by siRNA significantly inhibited U2OS and HOS cell proliferation and invasion, measured by CCK-8 and transwell assay. Besides, knockdown of RUSC1-AS1 increased cell apoptosis in osteosarcoma cell lines. In addition, RUSC1-AS1 promoted the epithelial-mesenchymal transition (EMT) process of osteosarcoma cells. In vivo experiments confirmed that RUSC1-AS1 knockdown had an inhibitory effect on osteosarcoma tumor growth. Mechanically, we showed that RUSC1-AS1 directly binds to and inhibits miR-340-5p and activates the PI3K/AKT signaling pathway. In conclusion, our study demonstrated that RUSC1-AS1 promoted osteosarcoma development both in vitro and in vivo through sponging to miR-340-5p and activating the PI3K/AKT signaling pathway. Therefore, RUSC1-AS1 becomes a potential therapeutic target for osteosarcoma.
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