ArticleJournal of translational medicine2025
GPX8 is transcriptionally regulated by KLF16 and promotes osteosarcoma progression.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundStudies have shown that glutathione peroxidase 8 (GPX8) promotes the progression of various cancers. However, the role of GPX8 in osteosarcoma (OS) progression remains unclear. The aim of this study was to investigate the function of GPX8 in OS progression and its underlying mechanisms.
methodsGPX8 expression in OS tissues and cell lines was assessed using immunohistochemistry (IHC), qRT‒PCR and Western blotting. The effects of GPX8 on the proliferative capacity of OS cells were evaluated using CCK-8, EdU, and plate colony formation assays. The role of GPX8 in the migratory and invasive functions of OS cells was examined via scratch wound healing, Transwell, and invasion assays. The effect of GPX8 on the in vivo proliferative ability of OS cells was investigated through a subcutaneous tumour formation experiment in nude mice. Bioinformatics methods were employed to predict the transcription factors that regulate GPX8 expression. Chromatin immunoprecipitation and dual-luciferase reporter assays were performed to investigate the interaction between GPX8 and Kruppel‑like factor 16 (KLF16).
resultsGPX8 is highly expressed in OS tissues and OS cell lines. Knocking down GPX8 expression significantly inhibited OS cell proliferation, migration, and invasion; downregulated CyclinD1 protein expression; and suppressed the EMT process. Conversely, GPX8 overexpression yielded the opposite results. Knocking down GPX8 expression significantly inhibited the tumorigenic ability of OS cells in vivo. KLF16 is highly expressed in OS tissues and cell lines. KLF16 promotes GPX8 expression. Knocking down GPX8 expression inhibited the promoting effects of KLF16 overexpression on OS cell proliferation, invasion, and migration, whereas overexpressing GPX8 reversed the inhibitory effects of KLF16 knockdown on OS cell proliferation, invasion, and migration. The results of the dual-luciferase and ChIP assays demonstrated that KLF16 directly binds to the GPX8 promoter and positively regulates GPX8 expression.
conclusionsThis study demonstrated that GPX8 is a critical oncogene in OS progression and that its expression is regulated by KLF16. Targeting the KLF16/GPX8 axis may offer promising prospects for the development of novel therapeutic strategies against OS.
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