NAMPT enhances LOX expression and promotes metastasis in human chondrosarcoma cells by inhibiting miR-26b-5p synthesis.
Chih-Yang LinYat-Yin LawCheng-Chieh YuYu-Ying WuSheng-Mou HouWei-Li ChenShang-Yu YangChun-Hao TsaiYuan-Shun LoYi-Chin FongChih-Hsin TangPublished in: Journal of cellular physiology (2024)
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.
Keyphrases
- induced apoptosis
- signaling pathway
- gene expression
- end stage renal disease
- cell cycle arrest
- endothelial cells
- cell proliferation
- poor prognosis
- single cell
- chronic kidney disease
- dna methylation
- low density lipoprotein
- stem cells
- oxidative stress
- epithelial mesenchymal transition
- bone mineral density
- pi k akt
- body composition
- mesenchymal stem cells
- cell therapy
- tyrosine kinase
- pluripotent stem cells
- induced pluripotent stem cells