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Updated: Jun 25, 2025

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Visfatin Facilitates VEGF-D-Induced Lymphangiogenesis through Activating HIF-1α and Suppressing miR-2277-3p in Human

Chang-Yu Song1, Shang-Lin Hsieh1,2, Shang-Yu Yang3

  • 1Graduate Institute of Biomedical Science, China Medical University, Taichung 40402, Taiwan.

International Journal of Molecular Sciences
|May 25, 2024
PubMed
Summary

Visfatin promotes chondrosarcoma metastasis by increasing VEGF-D and lymphangiogenesis. Targeting visfatin may offer a new treatment strategy for chondrosarcoma, a bone cancer linked to lung spread.

Keywords:
HIF1αVEGF-DchondrosarcomalymphangiogenesismiR-2277-3p

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Chondrosarcoma, a malignant bone tumor, is characterized by cartilaginous abnormalities and a propensity for lung metastasis.
  • Lymphangiogenesis, the formation of new lymphatic vessels, is crucial for cancer spread.
  • Visfatin, an adipokine, is implicated in tumor metastasis, but its role in chondrosarcoma lymphangiogenesis and VEGF-D production is unclear.

Purpose of the Study:

  • To investigate the role of visfatin in VEGF-D production and lymphangiogenesis in chondrosarcoma.
  • To elucidate the molecular mechanisms by which visfatin influences VEGF-D generation and lymphatic endothelial cell activity.
  • To evaluate the therapeutic potential of targeting visfatin in chondrosarcoma.

Main Methods:

  • Analysis of VEGF-D levels in clinical chondrosarcoma samples.
  • In vitro studies stimulating lymphatic endothelial cells with visfatin.
  • Investigation of signaling pathways including HIF-1α, Raf/MEK/ERK, and miR-2277-3p.
  • In vivo experiments to assess visfatin's effect on chondrosarcoma lymphangiogenesis.

Main Results:

  • VEGF-D levels were significantly elevated in chondrosarcoma patients compared to normal individuals.
  • Visfatin stimulation enhanced VEGF-D-dependent lymphangiogenesis in lymphatic endothelial cells.
  • Visfatin increased VEGF-D production by activating HIF-1α and downregulating miR-2277-3p via the Raf/MEK/ERK pathway.
  • Visfatin demonstrated control over chondrosarcoma-related lymphangiogenesis in vivo.

Conclusions:

  • Visfatin plays a significant role in promoting chondrosarcoma lymphangiogenesis through VEGF-D.
  • The visfatin-induced pathway involves HIF-1α activation and modulation of miR-2277-3p via the Raf/MEK/ERK cascade.
  • Visfatin represents a potential therapeutic target for inhibiting lymphangiogenesis and metastasis in chondrosarcoma.