ArticleCell biochemistry and function2018
NAIF1 suppresses osteosarcoma progression and is regulated by miR-128.
Article in Cell biochemistry and function, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- MiR-1202 increases radioresistance in nasopharyngeal carcinoma by targeting NAIF1/MAPK/ERK pathway.iScience · 2026Article
- The neurodevelopmental gene MSANTD2 belongs to a gene family formed by recurrent molecular domestication of Harbinger transposons at the base of vertebrates.Molecular biology and evolution · 2022Article
- Protective effects of the notoginsenoside R1 on acute lung injury by regulating the miR-128-2-5p/Tollip signaling pathway in rats with severe acute pancreatitis.Innate immunity · 2022Article
- HIV-infection and cocaine use regulate semen extracellular vesicles proteome and miRNAome in a manner that mediates strategic monocyte haptotaxis governed by miR-128 network.Cellular and molecular life sciences : CMLS · 2021Article
- Article
- miRNA-128 modulates bone neoplasms cells proliferation and migration through the WNT/β-catenin and EMT signal pathways.Journal of orthopaedic surgery and research · 2021Article
- The effect of dexmedetomidine on biological behavior of osteosarcoma cells through miR-1307 expression.American journal of translational research · 2021Article
- NAIF1 suppresses osteosarcoma progression and is regulated by miR-128.Cell biochemistry and function · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nuclear apoptosis-inducing factor 1 (NAIF1) acts as an oncogene and involves in tumorigenesis in several cancers. However, the expression and mechanism of NAIF1 in osteosarcoma remains unclear. In this study, we demonstrated the downregulation of NAIF1 expression in both osteosarcoma tissues and cell lines. We next explored the potential role of NAIF1 in osteosarcoma cell proliferation and migration. The result showed that overexpression of NAIF1 evidently suppressed the cell proliferation and invasion of osteosarcoma. Furthermore, we investigated the potential mechanisms accounting for dysregulation of NAIF1 in osteosarcoma. The bioinformatic prediction and luciferase reporter assay revealed that miR-128 is a direct upstream regulator of NAIF1 and regulates NAIF1 expression by binding the 3'-UTR of NAIF1. Consistent with previous study, we found that miR-128 was upregulated in both osteosarcoma tissues and cell lines. Moreover, miR-128 expression levels were inversely correlated with that of NAIF1 in osteosarcoma tissues. Finally, functional assay showed that miR-128 significantly suppressed osteosarcoma progression partially mediated by inhibiting NAIF1 expression. These data indicate that the miR-128 and its target gene NAIF1 played important roles by regulating OS cell proliferation and migration phenotype. SIGNIFICANCE OF THE STUDY: Osteosarcoma (OS) is the most common malignant bone tumour and the second leading cause of cancer-related death affecting children and adolescents. Nuclear apoptosis-inducing factor 1 (NAIF1) plays an inhibitory role in the initial steps of different carcinomas. However, the expression and mechanism of NAIF1 in osteosarcoma remains unclear. The data of this study indicated that the miR-128 and its target gene NAIF1 played important roles by regulating OS cell proliferation and migration phenotype. It was demonstrated that NAIF1 would demonstrate important regulative effects and may be a promising therapeutic target of OS.
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