Aspirin suppresses the growth and metastasis of osteosarcoma through the NF-κB pathway
Menée sur des lignées cellulaires d'ostéosarcome et à l'aide de xénogreffes, cette étude met en évidence des mécanismes par lesquels, en régulant la voie de signalisation NF-kappaB, l'aspirine inhibe le processus métastatique
Purpose: Aspirin has recently been reported to reduce both the incidence and the risk of metastasis in colon cancer. However, there is no evidence at the cellular levels or in the animal models for such an effect of Aspirin on cancer metastasis. Experimental Design: MTT assay, colony formation assay and apoptosis assay were employed to analyze the effects of Aspirin on the osteosarcoma (OS) cell viability in vitro. The NF-kB activity was measured by the NF-kB p65 luciferase reporter. Western blotting was used to analyze the proteins in cells. The migration and invasion abilities of OS cells in vitro were measured by the transwell assay. Xenograft-bearing mice were used to assess the roles of Aspirin in both tumor growth and metastasis of OS in vivo (n = 5-8 mice per group). An unpaired student's t test or ANOVA with Bonferroni post hoc test were used for the statistical comparisons. Results: Aspirin reduced cell viability in a dose- and time-dependent manner in OS cell lines, and Aspirin synergistically sensitized OS cells to cisplatin (DDP) in vitro and in vivo (p < 0.001). Moreover, Aspirin markedly repressed the migration and invasion of OS cells in vitro (p < 0.001), and dramatically diminished the occurrence of OS xenograft metastases to the lungs in vivo (p < 0.001). Mechanistically, Aspirin diminishes OS migration, invasion and metastasis through the NF-kB pathway. Conclusion: Aspirin suppresses both the growth and metastasis of OS through the NF-kB pathway at the cellular level and in the animal models.