C-Met受体及其配体肝细胞生长因子（HGF）在多种骨肉瘤细胞系和骨肉瘤病理样本中均高表达。表明c-Met/HGF在骨肉瘤的发展中起重要作用。本研究旨在探索针对c-Met的药物吉西他滨对骨肉瘤（OS）细胞的抗癌作用。通过CCK8检测吉西他滨在不同浓度下对骨肉瘤细胞（SaOS2、MG-63和MNNG）的增殖效应。以人骨肉瘤细胞株MG-63作为体外模型，评估2.5 μM吉西他滨、5.0 μM吉西他滨和DMSO对细胞凋亡、细胞周期、迁移和侵袭的影响。通过Western blot检测骨肉瘤细胞中c-Met信号通路的表达情况。结果显示，吉西他滨呈浓度依赖性抑制细胞系的增殖。与对照组相比，吉西他滨显著增加了凋亡细胞数量。与对照组相比，吉西他滨增加了G0/G1期细胞数量，减少了S期细胞数量。与对照组相比，吉西他滨抑制了骨肉瘤细胞的迁移和侵袭，并降低了c-Met/Gab1/STAT5的表达。本研究将为吉西他滨在骨肉瘤的临床应用提供一个有希望的治疗靶点和理论依据。

C-Met receptor and its ligand hepatocyte growth factor (HGF) are overexpressed in a variety of osteosarcoma cell lines and osteosarcoma pathological samples. It is suggested that c-Met/HGF plays an important role in the development of osteosarcoma. This study aimed to explore the anticancer effect of the c-Met-targeted drug crizotinib on osteosarcoma (OS) cells. The effects of crizotinib on the proliferation of osteosarcoma cells (SaOS2, MG-63 and MNNG) at different concentrations were detected by CCK8. Human osteosarcoma cell line MG-63 was used as an in vitro model to evaluate the effects of 2.5 μM crizotinib, 5.0 μM crizotinib and DMSO on cell apoptosis, cell cycle, migration and invasion. The expression of the c-Met signaling pathway in osteosarcoma cells was detected by western blot. The results showed that crizotinib inhibited the proliferation of cell lines in a concentration-dependent manner. Crizotinib significantly increased the number of apoptotic cells compared with the control group. Compared with the control group, crizotinib increased G0/G1 phase cells and decreased S phase cells. Compared with the control group, crizotinib inhibited the migration and invasion of osteosarcoma cells and decreased the expression of c-Met/Gab1/STAT5. This study will provide a promising therapeutic target and theoretical basis for the clinical application of crizotinib in osteosarcoma.