<p>miR-100-5p Inhibits Malignant Behavior of Chordoma Cells by Targeting IGF1R</p>

• DOI: 10.2147/cmar.s252185
• Publication Date: 2020-06-01T22:59:18Z
• Authors: Hongliang Zhang; Kang Yang; Tingting Ren; Yi Huang; Xin Liang; Yiyang Yu; Wei Wang; Jianfang Niu; Jingbing Lou; Xiaodong Tang; Wei Guo
• Keywords: 0301 basic medicine; 03 medical and health sciences; Cancer Management and Research; igf1r; Neoplasms. Tumors. Oncology. Including cancer and carcinogens; chordoma; mir-100-5p; RC254-282; mirna; Original Research

Our research aimed to illuminate the role of miR-100-5p in chordoma and potential mechanism.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.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.In conclusion, our results showed that miR-100-5p was lowly expressed in chordoma and inhibited tumor malignant progression by targeting IGF1R.