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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Bone Neoplasms, Cell Cycle, Cell Cycle Checkpoints, Cell Cycle Proteins, Cell Line, Tumor, Cell Proliferation, Gene Silencing, Humans, Osteosarcoma, RNA, Small Interfering.
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Does silencing of NUF2 inhibit proliferation of human osteosarcoma Saos-2 cells? Context: NUF2 (NUF2, Ndc80 kinetochore complex component), which is essential for kinetochore-microtubule attachment in mitosis, has emerged as a critical mediator of the cell cycle in multiple tumour occurrences. In the present study, we aimed to investigate the role of NUF2 in osteosarcoma, one of the most common primary bone tumours in children and young adults. Lentivirus-mediated short-hairpin RNA (shRNA) targeting NUF2 (Lv-shNUF2) was employed for evaluation in human osteosarcoma Saos-2 cells. After NUF2 silencing, the proliferation of Saos-2 cells was significantly inhibited, as determined by the MTT assay. The colony forming ability was also significantly decreased in Saos-2 cells infected with Lv-shNUF2. Flow cytometry revealed that downregulation of NUF2 in Saos-2 cells caused a remarkable accumulation of the cell population in the S phase. Furthermore, the expression levels of cell cycle regulators cyclin A and cyclin-dependent kinase 2 (CDK2) were notably decreased, whereas those of cyclin-dependent kinase inhibitors p21Cip1 and p27Kip1, were increased in response to NUF2 knockdown in Saos-2 cells.
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Our findings suggest that NUF2 might modulate cell proliferation via cell cycle control in Saos-2 cells. Downregulation of NUF2 by shRNA might be a novel strategy for early treatment of osteosarcoma using molecular-targeting therapy. Final Decision: yes