ArticleFrontiers in cell and developmental biology2020
NDUFA4L2 Regulated by HIF-1α Promotes Metastasis and Epithelial-Mesenchymal Transition of Osteosarcoma Cells Through Inhibiting ROS Production.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 33 citations in OpenAlex.
- Integrating weighted gene co-expression network analysis and machine learning reveal that NDUFA4L2 alleviates KA-induced HT22 cell neurotoxicity, apoptosis, oxidative stress, and mitochondrial dysfunction.Journal of bioenergetics and biomembranes · 2026Article
- Depleting HIF‑1α attenuates the progression of osteosarcoma, but tumorigenicity is sustained through HIF‑independent pathways.Oncology reports · 2026Article
- A Review of HIF-1α-Mediated Integration of Metabolic Reprogramming, Mitochondrial Function, and PI3K/Akt-MAPK-Nrf2-NF-κB Signaling.Antioxidants (Basel, Switzerland) · 2026Review
- Genomic Insights into the Origins, Population Structure, and Local Adaptation of Philippine Visayan Native Cattle.Animals : an open access journal from MDPI · 2026Article
- Metabolic reprogramming and immune evasion interaction in the tumor microenvironment promote tumor progression.Frontiers in oncology · 2026Review
- Ectopic expression of GDF15 in cancer-associated fibroblasts enhances melanoma immunosuppression via the GFRAL/RET cascade.Journal for immunotherapy of cancer · 2025Article
- 3D-printed β-TCP scaffold as a bone-mimicking environment for an engineered model of osteosarcoma:Materials today. Bio · 2025Article
- The Recruitment and Immune Suppression Mechanisms of Myeloid-Derived Suppressor Cells and Their Impact on Bone Metastatic Cancer.Cancer reports (Hoboken, N.J.) · 2025Review
- Deciphering MARCH5's impact on multiple myeloma: insights into autophagy regulation and AKT-FOXO3 signaling.Blood neoplasia · 2024Article
- Pancancer analysis of NDUFA4L2 with focused role in tumor progression and metastasis of colon adenocarcinoma.Medical oncology (Northwood, London, England) · 2024Article
- Revisiting reactive oxygen species production in hypoxia.Pflugers Archiv : European journal of physiology · 2024Review
- Lipid Peroxidation-Related Redox Signaling in Osteosarcoma.International journal of molecular sciences · 2024Review
- Advances in prognostic models for osteosarcoma risk.Heliyon · 2024Review
- Novel Ultrastructural Insights into the Clear-Cell Carcinoma of the Pancreas: A Case Report.International journal of molecular sciences · 2024Article
- Article
- Immunometabolism of ferroptosis in the tumor microenvironment.Frontiers in oncology · 2024Review
- Hypoxia-induced the upregulation of NDUFA4L2 promoted colon adenocarcinoma progression through ROS-mediated PI3K/AKT pathway.Cytotechnology · 2023Article
- Review
- Involvement of redox signalling in tumour cell dormancy and metastasis.Cancer metastasis reviews · 2023Review
- Transcriptional regulation of NDUFA4L2 by NFIB induces sorafenib resistance by decreasing reactive oxygen species in hepatocellular carcinoma.Cancer science · 2023Article
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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
Osteosarcoma (OS) accounts for a large proportion of the types of bone tumors that are newly diagnosed, and is a relatively common bone tumor. However, there are still no effective treatments for this affliction. One interesting avenue is related to the mitochondrial NDUFA4L2 protein, which is encoded by the nuclear gene and is known to be a critical mediator in the regulation of cell survival. Thus, in this study, we aimed to investigate the effect of NDUFA4L2 upon the metastasis and epithelial-mesenchymal transition of OS. We found that NDUFA4L2 protein expression was upregulated in hypoxic conditions. We also used 2-ME and DMOG, which are HIF-1α inhibitors and agonists, respectively, to assess the effects related to decreasing or increasing HIF-1α expression. 2-ME caused a significant decrease of NDUFA4L2 expression and DMOG had the opposite effect. It was obvious that down-regulation of NDUFA4L2 had a direct interaction with the apoptosis of OS cells. Western blotting, wound healing analyses, Transwell invasion assays, and colony formation assays all indicated and supported the conclusion that NDUFA4L2 promoted OS cell migration, invasion, proliferation, and the epithelial-mesenchymal transition. During experiments, we incidentally discovered that autophagy and the ROS inhibitor could be used to facilitate the rescuing of tumor cells whose NDUFA4L2 was knocked down. Our findings will help to further elucidate the dynamics underlying the mechanism of OS cells and have provided a novel therapeutic target for the treatment of OS.
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