부산대학교 도서관

Hongliang Zhang,1,2 Kang Yang,3 Tingting Ren,1,2 Yi Huang,1,2 Xin Liang,1,2 Yiyang Yu,1,2 Wei Wang,1,2 Jianfang Niu,1,2 Jingbing Lou,1,2 Xiaodong Tang,1,2 Wei Guo1,2 1Musculoskeletal Tumor Center, Peking University People’s Hospital, Beijing, People’s Republic of China; 2Beijing Key Laboratory of Musculoskeletal Tumor, Beijing, People’s Republic of China; 3Department of Orthopedics, Yangzhou University Affiliated Hospital, Yangzhou, People’s Republic of ChinaCorrespondence: Xiaodong Tang; Wei GuoMusculoskeletal Tumor Center, Peking University People’s Hospital, No. 11 Xizhimen South Street, Beijing 100044, People’s Republic of ChinaTel +86 10 8832 4471Fax +86.10.8837.8544Email tang15877@163.com; guobonetumor@163.comPurpose: Our research aimed to illuminate the role of miR-100-5p in chordoma and potential mechanism.Materials and Methods: We used microRNA array analysis to explore differentially expressed miRNAs in chordoma tissue and then verified by qRT-PCR. Cell proliferation and transwell assay were used to evaluate the function of miR-100-5p. Cell apoptosis was analyzed by flow cytometry, and using biological software, we predicted that the insulin-like growth factor 1 receptor (IGF1R) could be the target gene of miR-100-5p, which was then validated by dual luciferase assays and Western blot.Results: miR-100-5p was downregulated in chordoma tissues. Overexpression of miR-100-5p could suppress the growth of chordoma both in vitro and in vivo, and miR-100-5p could inhibit the migration and invasion of chordoma cells partially by suppressing epithelial–mesenchymal transition (EMT). Furthermore, IGF1R was validated as the target gene of miR-100-5p and expressed in most chordoma tissues.Conclusion: In conclusion, our results showed that miR-100-5p was lowly expressed in chordoma and inhibited tumor malignant progression by targeting IGF1R.Keywords: chordoma, miRNA, miR-100-5p, IGF1R