Abstract
BackgroundThis article reports the effects of proenkephalin (PENK) on osteosarcoma (OS) cell migration.MethodsA Gene Expression Omnibus (GEO) dataset was used to identify differentially expressed genes (DEGs) in OS tumor samples and normal human osteoblasts. Tumor tissue and adjacent normal tissue were collected from 40 OS patients. MG63 cells were transfected with si-PENK. Transwell migration assays and wound healing assays were performed to compare the effect of PENK on migration. Moreover, LY294002 was used to identify the potential mechanism. Gene expression was examined via qRT-PCR and Western blotting.ResultsBioinformatic analysis revealed that PENK was downregulated in OS tumor samples compared with normal human osteoblasts. Moreover, PENK was identified as the hub gene of the DEGs. The PI3K/Akt signaling pathway was significantly enriched in the DEGs. Moreover, PENK was downregulated in OS and MG63 cells compared with the corresponding control cells. Silencing PENK promoted MG63 cell migration; however, treatment with LY294002 partially attenuated PENK silencing-induced OS cell migration.ConclusionPENK inhibits OS cell migration by activating the PI3K/Akt signaling pathway.
Highlights
Osteosarcoma (OS), a tumor of mesenchymal origin, is a common bone malignancy [1, 2]
Gene Ontology (GO) term enrichment analysis was used to annotate the enrichment of the differentially expressed genes (DEGs) in gene functional terms in the molecular function (MF), biological process (BP), and cellular component (CC) categories
The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis results revealed that the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway was enriched in the DEGs
Summary
Osteosarcoma (OS), a tumor of mesenchymal origin, is a common bone malignancy [1, 2]. OS is characterized by direct formation of osteoid tissue or immature bone by tumor cells [3] and accounts for approximately 60% of pediatric bone tumors [4]. Traditional treatment strategies for OS mainly include medical approaches such as multidrug chemotherapy and wide surgical excision [5]. The inhibitory effect of these strategies on the progression of OS is limited. Exploring the hub genes involved in OS could help identify therapeutic targets for OS. Previous studies identified FGF5 as an early diagnostic marker for OS [7]. No core gene that could be a therapeutic target for OS has been identified. This article reports the effects of proenkephalin (PENK) on osteosarcoma (OS) cell migration
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