ArticleJournal of applied biomedicine2021
The NF-κB pathway is critically implicated in the oncogenic phenotype of human osteosarcoma cells.
Article in Journal of applied biomedicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Article
- Targeting myeloid-derived suppressor cells in the tumor microenvironment: potential therapeutic approaches for osteosarcoma.Oncology research · 2025Review
- Review
- Reprogramming of glucose metabolism: Metabolic alterations in the progression of osteosarcoma.Journal of bone oncology · 2024Review
- Toll-like receptor 4 signaling in osteoblasts is required for load-induced bone formation in mice.iScience · 2023Article
- Reinforcement of Sorafenib Anti-osteosarcoma Effect by Amentoflavone Is Associated With the Induction of Apoptosis and Inactivation of ERK/NF-κB.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NF-κB is activated in a variety of human cancers. However, its role in osteosarcoma (OS) remains unknown. Here, we have elucidated the implication of NF-κB in the oncogenic phenotype of OS tumor cells. We reported that activation of NF-κB was a common event in the human OS. Inhibition of NF-κB using inhibitor Bay 11-7085 repressed proliferation, survival, migration, and invasion but increased apoptosis in 143B and MG63 OS cells, indicating that NF-κB is critically implicated in the oncogenesis of OS. Notably, Bay 11-7085 not only inactivated NF-κB but also reduced the phosphorylation of AKT via its induction of PTEN, suggesting the existence of a novel NF-κB/PTEN/PI3K/AKT axis. In vivo, Bay 11-7085 suppressed tumor growth in the bone by targeting NF-κB and AKT. Interestingly, combined treatment with Bay 11-7085 and the PI3K inhibitor, LY294002, triggered an augmented antitumor effect. Our results demonstrate that NF-κB potentiates the growth and aggressiveness of OS. Pharmacological inhibition of NF-κB represents a promising therapy for the treatment of OS.
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Registered trials
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