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Related Experiment Video

Updated: Dec 10, 2025

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MEX3C promotes osteosarcoma malignant progression through negatively regulating FGF14.

Yile Cao1, Fan Jiang, Sheng Zhang

  • 1Department of Clinical Medicine, Yangzhou University Medical College, Yangzhou 225000, China.

Journal of B.U.ON. : Official Journal of the Balkan Union of Oncology
|August 31, 2020
PubMed
Summary

The oncogene MEX3C promotes osteosarcoma (OS) progression by downregulating FGF14. This study reveals MEX3C as a potential therapeutic target for inhibiting OS metastasis.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • MEX3C is implicated as an oncogene in various cancers.
  • Its specific role in osteosarcoma (OS) development and metastasis remains largely unexplored.
  • Understanding MEX3C's function is crucial for developing novel therapeutic strategies for OS.

Purpose of the Study:

  • To investigate the role of MEX3C in the malignant progression of osteosarcoma (OS).
  • To explore the potential regulatory relationship between MEX3C and FGF14 in OS.
  • To determine if MEX3C influences OS cell migration and invasion.

Main Methods:

  • Quantitative real-time polymerase chain reaction (qRT-PCR) to assess MEX3C and FGF14 expression in OS tissues and cell lines.
  • Construction of MEX3C overexpression and knockdown cell models in HOS and MG63 OS cells.
  • Cell migration and invasion assays (wound healing and Transwell assays).
  • Luciferase assay, Western blot, and recovery experiments to confirm MEX3C-FGF14 interaction.

Main Results:

  • MEX3C expression was significantly elevated in OS tissues and cell lines compared to adjacent tissues.
  • High MEX3C expression correlated with increased incidence of nodal involvement and distant metastasis in OS patients.
  • MEX3C knockdown reduced OS cell migration and invasion, while overexpression enhanced these processes.
  • MEX3C directly binds to FGF14, leading to decreased FGF14 expression in OS.
  • FGF14 overexpression reversed the pro-migratory and invasive effects of MEX3C.

Conclusions:

  • MEX3C is upregulated in osteosarcoma and is associated with a higher risk of metastasis.
  • MEX3C accelerates OS malignant progression by negatively regulating FGF14.
  • Targeting the MEX3C/FGF14 pathway may offer a novel therapeutic approach for osteosarcoma.