MiR-150-5p inhibits cell proliferation and metastasis by targeting FTO in osteosarcoma.

IF 2 4区 医学 Q3 ONCOLOGY Oncology Research Pub Date : 2024-10-16 eCollection Date: 2024-01-01 DOI:10.32604/or.2024.047704
Lichen Xu, Pan Zhang, Guiqi Zhang, Zhaoliang Shen, Xizhuang Bai
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Abstract

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.

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MiR-150-5p 通过靶向 FTO 抑制骨肉瘤的细胞增殖和转移
背景:骨肉瘤(Osteosarcoma,OS)被认为是源自骨骼的最主要恶性肿瘤,有必要深入了解其内在机制,以确定新的治疗靶点并改进治疗方法。材料与方法:1.分析肿瘤中 FTO 的表达和存活率。2.2. 利用 Western 印迹和 PCR 对 OS 细胞系中的 FTO 进行定量分析。3.3. FTO在MG63中分别上调和下调。4.4. 利用 CCK-8、集落形成、伤口愈合和 Transwell 试验评估 FTO 对 OS 细胞增殖和迁移的影响。5.5. 确定了miR-150-5p在OS细胞外泌体中的表达。6.通过 TargetScan 预测了 miR-150-5p 与 FTO 的结合,并通过荧光素酶报告实验证实了这一点。7.7. 研究了外泌体 miR-150-5p 对 OS 细胞增殖和迁移的影响:结果:与正常组织相比,FTO在OS组织中的表达量更高,这与存活率较低有关。此外,下调 FTO 能显著抑制 OS 细胞的生长和转移。此外,通过双荧光素酶实验发现,在OS细胞及其衍生外泌体中均下调的miR-150-5p与FTO的3'-UTR结合。外泌体miR-150-5p可降低FTO的表达并抑制细胞活力:结论:我们发现 OS 中 FTO 水平升高,这可能与细胞和外泌体中 miR-150-5p 水平不足有关。这表明,miR-150-5p 的失调及其与 FTO 的相互作用可能会促进 OS 的发展。
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来源期刊
Oncology Research
Oncology Research 医学-肿瘤学
CiteScore
4.40
自引率
0.00%
发文量
56
审稿时长
3 months
期刊介绍: Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.
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