Open Access

ARTICLE

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

LICHEN XU^1,2, PAN ZHANG^3,*, GUIQI ZHANG², ZHAOLIANG SHEN⁴, XIZHUANG BAI^1,3,*

1 Dalian Medical University, Dalian, 116044, China
2 Department of Spinal Surgery, Dalian Municipal Central Hospital, Dalian, 116033, China
3 Department of Orthopaedics, The People’s Hospital of China Medical University, People’s Hospital of Liaoning Province, Shenyang, 110016, China
4 Department of Orthopedic, The Third Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, China

* Corresponding Authors: PAN ZHANG. Email: ; XIZHUANG BAI. Email:

Oncology Research 2024, 32(11), 1777-1789. https://doi.org/10.32604/or.2024.047704

Received 14 November 2023; Accepted 07 April 2024; Issue published 16 October 2024

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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