1. NAMPT enhances LOX expression and promotes metastasis in human chondrosarcoma cells by inhibiting miR-26b-5p synthesis.
- Author
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Lin CY, Law YY, Yu CC, Wu YY, Hou SM, Chen WL, Yang SY, Tsai CH, Lo YS, Fong YC, and Tang CH
- Subjects
- Humans, Cell Line, Tumor, Signal Transduction, Lung Neoplasms genetics, Lung Neoplasms pathology, Lung Neoplasms metabolism, Animals, Proto-Oncogene Proteins c-akt metabolism, Proto-Oncogene Proteins c-akt genetics, Male, Mice, Nude, Chondrosarcoma genetics, Chondrosarcoma pathology, Chondrosarcoma metabolism, Nicotinamide Phosphoribosyltransferase genetics, Nicotinamide Phosphoribosyltransferase metabolism, MicroRNAs genetics, MicroRNAs metabolism, Gene Expression Regulation, Neoplastic genetics, Protein-Lysine 6-Oxidase metabolism, Protein-Lysine 6-Oxidase genetics, Cell Movement genetics, Bone Neoplasms genetics, Bone Neoplasms pathology, Bone Neoplasms metabolism, Cytokines metabolism, Cytokines genetics
- Abstract
Chondrosarcoma is a malignant bone tumor that emerges from abnormalities in cartilaginous tissue and is related with lung metastases. Nicotinamide phosphoribosyltransferase (NAMPT) is an adipocytokine reported to enhance tumor metastasis. Our results from clinical samples and the Gene Expression Omnibus data set reveal that NAMPT levels are markedly higher in chondrosarcoma patients than in normal individuals. NAMPT stimulation significantly increased lysyl oxidase (LOX) production in chondrosarcoma cells. Additionally, NAMPT increased LOX-dependent cell migration and invasion in chondrosarcoma by suppressing miR-26b-5p generation through the c-Src and Akt signaling pathways. Overexpression of NAMPT promoted chondrosarcoma metastasis to the lung in vivo. Furthermore, knockdown of LOX counteracted NAMPT-facilitated metastasis. Thus, the NAMPT/LOX axis presents a novel target for treating the metastasis of chondrosarcoma., (© 2024 Wiley Periodicals LLC.)
- Published
- 2024
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