Visfatin Facilitates VEGF-D-Induced Lymphangiogenesis Through Activating HIF-1α and Suppressing MiR-2277-3p in Human Chondrosarcoma

Overview

Journal Int J Mol Sci

Publisher MDPI

Specialties Biochemistry
Chemistry
Molecular Biology

Date 2024 May 25

PMID 38791180

Authors

Chang-Yu Song

Shang-Lin Hsieh

Shang-Yu Yang

Chih-Yang Lin

Shih-Wei Wang

Chun-Hao Tsai

Yuan-Shun Lo

Yi-Chin Fong

Chih-Hsin Tang

Affiliations

Soon will be listed here.

Abstract

Chondrosarcoma is a malignant bone tumor that arises from abnormalities in cartilaginous tissue and is associated with lung metastases. Lymphangiogenesis plays an essential role in cancer metastasis. Visfatin is an adipokine reported to enhance tumor metastasis, but its relationship with VEGF-D generation and lymphangiogenesis in chondrosarcoma remains undetermined. Our results from clinical samples reveal that VEGF-D levels are markedly higher in chondrosarcoma patients than in normal individuals. Visfatin stimulation promotes VEGF-D-dependent lymphatic endothelial cell lymphangiogenesis. We also found that visfatin induces VEGF-D production by activating HIF-1α and reducing miR-2277-3p generation through the Raf/MEK/ERK signaling cascade. Importantly, visfatin controls chondrosarcoma-related lymphangiogenesis in vivo. Therefore, visfatin is a promising target in the treatment of chondrosarcoma lymphangiogenesis.

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