PNO1 promotes the progression of osteosarcoma via TGF-β and YAP/TAZ pathway

Abstract

Abstract This study aimed to explore the potential role and mechanisms of the partner of NOB1 homolog (PNO1) in osteosarcoma. The expression of PNO1 in tumor and adjacent tissue samples was examined using western blotting. Lentiviral transfection was used to establish sh-Ctrl and sh-PNO1 osteosarcoma cell lines. MTT assay, Celigo cell cytometer count, and cell colony formation assay were used to investigate the proliferation of osteosarcoma cells in vitro, whereas xenotransplantation assay was performed for in vivo experiments. Wound-healing and Transwell assays were chosen to verify the migration and invasion of osteosarcoma cells. Flow cytometry assay and caspase-3/7 activity analysis were adopted for the analysis of cell apoptosis and cell cycle. Finally, transcriptome sequencing and bioinformatics analysis were adopted to explore the acting mechanisms. The expression of PNO1 was higher in osteosarcoma tissues than that in adjacent tissues. Down-regulation of PNO1 inhibited the proliferation, migration, and invasion, and induced cell apoptosis and cell cycle arrest of osteosarcoma cells. Furthermore, according to transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes pathway analysis, we found that PNO1 might affect the progression of osteosarcoma via TGF-β and YAP/TAZ signaling pathways. PNO1 could be a potential target for osteosarcoma treatment.