miR-584-5p Inhibits Osteosarcoma Progression by Targeting Connective Tissue Growth Factor.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2023-11-01 Epub Date: 2022-01-17 DOI:10.1089/cbr.2021.0349
Qian Lu, Yongli Wang, Xuesheng Jiang, Sheng Huang
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引用次数: 2

Abstract

Background: miR-584-5p is a critical regulator in the progression of multiple cancers. However, its specific role and downstream targets in osteosarcoma are unclear. This research investigated the roles and underlying mechanisms of miR-769-5p and the Hippo pathway in osteosarcoma cells. Materials and Methods: RT-qPCR, CCK-8 and EdU and colony formation, wound-healing and transwell chamber, flow cytometry, and Western blot assay detected the expression of miR-584-5p and CTGF, cell proliferation, migration, invasion apoptosis and protein expression. Result: Their study illuminated that miR-584-5p overexpression repressed osteosarcoma cell migration/invasion and proliferation and facilitated apoptosis. Mechanistically, miR-584-5p targets negatively regulated connective tissue growth factor (CTGF). miR-584-5p inhibited osteosarcoma cell metastasis by regulating CTGF. In addition, miR-584-5p inactivated the Hippo pathway through CTGF in osteosarcoma. Conclusion: miR-584-5p inhibits osteosarcoma cell proliferation, migration, and invasion and promotes apoptosis by targeting CTGF, indicating that miR-584-5p acts as a promising diagnostic and predictive biomarker for osteosarcoma.

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miR-584-5p通过靶向结缔组织生长因子抑制骨肉瘤进展
背景:miR-584-5p是多种癌症进展的关键调节因子。然而,其在骨肉瘤中的具体作用和下游靶点尚不清楚。本研究探讨了miR-769-5p和Hippo通路在骨肉瘤细胞中的作用和潜在机制。材料与方法:RT-qPCR、CCK-8、EdU及集落形成、创面愈合及transwell室、流式细胞术、Western blot检测miR-584-5p、CTGF表达、细胞增殖、迁移、侵袭凋亡及蛋白表达。结果:他们的研究表明,miR-584-5p过表达抑制骨肉瘤细胞的迁移/侵袭和增殖,促进细胞凋亡。在机制上,miR-584-5p靶向负调节的结缔组织生长因子(CTGF)。miR-584-5p通过调节CTGF抑制骨肉瘤细胞转移。此外,miR-584-5p在骨肉瘤中通过CTGF灭活Hippo通路。结论:miR-584-5p通过靶向CTGF抑制骨肉瘤细胞增殖、迁移和侵袭,促进细胞凋亡,提示miR-584-5p是一种有前景的骨肉瘤诊断和预测生物标志物。
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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