Background:Osteosarcoma(OS),recognized as the predominant malignant tumor originating from bones,necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance tre...Background:Osteosarcoma(OS),recognized as the predominant malignant tumor originating from bones,necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance treatment methodologies.The role of fat mass and obesity-associated(FTO)in OS,particularly its correlation with malignant traits,and the fundamental mechanism,remains to be elucidated.Materials and Methods:1.The FTO expression and survival rate in tumors were analyzed.2.FTO in OS cell lines was quantified utilizing western blot and PCR.3.FTO was upregulated and downregulated separately in MG63.4.The impact of FTO on the proliferation and migration of OS cells was evaluated using CCK-8,colony formation,wound healing,and Transwell assays.5.The expression of miR-150-5p in OS cells-derived exosomes was identified.6.The binding of miR-150-5p to FTO was predicted by TargetScan and confirmed by luciferase reporter assay.7.The impact of exosome miR-150-5p on the proliferation and migration of OS cells was investigated.Results:The expression of FTO was higher in OS tissues compared to normal tissues correlating with a worse survival rate.Furthermore,the downregulation of FTO significantly impeded the growth and metastasis of OS cells.Additionally,miR-150-5p,which was downregulated in both OS cells and their derived exosomes,was found to bind to the 3′-UTR of FTO through dual luciferase experiments.Exosomal miR-150-5p was found to decrease the expression of FTO and inhibit cell viability.Conclusions:We identified elevated levels of FTO in OS,which may be attributed to insufficient miR-150-5p levels in both the cells and exosomes.It suggests that the dysregulation of miR-150-5p and its interaction with FTO could potentially promote the development of OS.展开更多
目的本研究旨在阐明miR-150在肝细胞癌(hepatocellular carcinoma,HCC)中的作用和靶点。方法采用热图分析方法,从癌症基因组图谱(The Cancer Genome Atlas)数据库下载的6组HCC组织与邻近肝组织之间差异表达的miRNA。采用实时定量聚合酶...目的本研究旨在阐明miR-150在肝细胞癌(hepatocellular carcinoma,HCC)中的作用和靶点。方法采用热图分析方法,从癌症基因组图谱(The Cancer Genome Atlas)数据库下载的6组HCC组织与邻近肝组织之间差异表达的miRNA。采用实时定量聚合酶链反应检测miR-150在HCC组织和细胞系中的表达;采用侵袭小室试验评估HCC细胞的增殖、侵袭和迁移潜能。此外,利用TargetScan软件用于预测miR-150的潜在靶标,并通过蛋白印迹(Western blotting)和荧光素酶法测定miR-150与其靶基因的关系。结果通过热图分析法,发现在HCC组织中有31个miRNA表达异常,其中miR-150表达差异最为显著,且与患者预后密切相关。细胞实验上,高表达miR-150可通过调节胰岛素样生长因子2-mRNA结合蛋白2(recombinant insulin like growth factor 2 mRNA binding protein 2,IGF2BP2)的表达显著降低人肝癌细胞株SMMC-7721和HepG2细胞的增殖、迁移和侵袭能力。结论miR-150通过调控IGF2BP2抑制HCC细胞的增殖、迁移和侵袭,为HCC提供了新的治疗靶点。展开更多
文摘Background:Osteosarcoma(OS),recognized as the predominant malignant tumor originating from bones,necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance treatment methodologies.The role of fat mass and obesity-associated(FTO)in OS,particularly its correlation with malignant traits,and the fundamental mechanism,remains to be elucidated.Materials and Methods:1.The FTO expression and survival rate in tumors were analyzed.2.FTO in OS cell lines was quantified utilizing western blot and PCR.3.FTO was upregulated and downregulated separately in MG63.4.The impact of FTO on the proliferation and migration of OS cells was evaluated using CCK-8,colony formation,wound healing,and Transwell assays.5.The expression of miR-150-5p in OS cells-derived exosomes was identified.6.The binding of miR-150-5p to FTO was predicted by TargetScan and confirmed by luciferase reporter assay.7.The impact of exosome miR-150-5p on the proliferation and migration of OS cells was investigated.Results:The expression of FTO was higher in OS tissues compared to normal tissues correlating with a worse survival rate.Furthermore,the downregulation of FTO significantly impeded the growth and metastasis of OS cells.Additionally,miR-150-5p,which was downregulated in both OS cells and their derived exosomes,was found to bind to the 3′-UTR of FTO through dual luciferase experiments.Exosomal miR-150-5p was found to decrease the expression of FTO and inhibit cell viability.Conclusions:We identified elevated levels of FTO in OS,which may be attributed to insufficient miR-150-5p levels in both the cells and exosomes.It suggests that the dysregulation of miR-150-5p and its interaction with FTO could potentially promote the development of OS.
文摘目的本研究旨在阐明miR-150在肝细胞癌(hepatocellular carcinoma,HCC)中的作用和靶点。方法采用热图分析方法,从癌症基因组图谱(The Cancer Genome Atlas)数据库下载的6组HCC组织与邻近肝组织之间差异表达的miRNA。采用实时定量聚合酶链反应检测miR-150在HCC组织和细胞系中的表达;采用侵袭小室试验评估HCC细胞的增殖、侵袭和迁移潜能。此外,利用TargetScan软件用于预测miR-150的潜在靶标,并通过蛋白印迹(Western blotting)和荧光素酶法测定miR-150与其靶基因的关系。结果通过热图分析法,发现在HCC组织中有31个miRNA表达异常,其中miR-150表达差异最为显著,且与患者预后密切相关。细胞实验上,高表达miR-150可通过调节胰岛素样生长因子2-mRNA结合蛋白2(recombinant insulin like growth factor 2 mRNA binding protein 2,IGF2BP2)的表达显著降低人肝癌细胞株SMMC-7721和HepG2细胞的增殖、迁移和侵袭能力。结论miR-150通过调控IGF2BP2抑制HCC细胞的增殖、迁移和侵袭,为HCC提供了新的治疗靶点。
