ArticleIn vitro cellular & developmental biology. Animal2019
NFKB1-miR-612-FAIM2 pathway regulates tumorigenesis in neurofibromatosis type 1.
Article in In vitro cellular & developmental biology. Animal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- NFKB1 as a key player in Tumor biology: from mechanisms to therapeutic implications.Cell biology and toxicology · 2025Pooled it
- Regulation of ER Stress-Associated Gene Expression by Lifeguard in Human Breast Cancer Cells.Cancer reports (Hoboken, N.J.) · 2026Article
- Circulating Extracellular Vesicles microRNAs Are Altered in Women Undergoing Preterm Birth.International journal of molecular sciences · 2023Article
- NEAT1 can be a diagnostic biomarker in the breast cancer and gastric cancer patients by targeting XIST, hsa-miR-612, and MTRNR2L8: integrated RNA targetome interaction and experimental expression analysis.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022Article
- Pharmacological Approaches in Neurofibromatosis Type 1-Associated Nervous System Tumors.Cancers · 2021Review
- Simultaneous microRNA-612 restoration and 5-FU treatment inhibit the growth and migration of human PANC-1 pancreatic cancer cells.EXCLI journal · 2021Article
- FAIM2 Promotes Non-Small Cell Lung Cancer Cell Growth and Bone Metastasis by Activating the Wnt/β-Catenin Pathway.Frontiers in oncology · 2021Article
- Naringin Targets NFKB1 to Alleviate Oxygen-Glucose Deprivation/Reoxygenation-Induced Injury in PC12 Cells Via Modulating HIF-1α/AKT/mTOR-Signaling Pathway.Journal of molecular neuroscience : MN · 2021Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurofibromatosis type I (NF1) is a carcinoma mainly featured by malignant peripheral nerve sheath tumor (MPNST). Dysregulated microRNAs (miRNAs) play decisive roles in tumor initiation and development. Our study sought for the possible roles of miR-612 in NF1. RT-qPCR estimated the expression of nuclear factor kappa B subunit 1 (NFKB1), miR-612, and Fas apoptotic inhibitory molecule 2 (FAIM2) in NF1, separately. Cell proliferation and migration were detected by CCK-8 and transwell experiments. Cell apoptosis was measured via flow cytometry and detection of the expression and activity of caspase 3/8/9. Luciferase reporter, ChIP, and RIP assays testified the interplay between studied genes. Rescue and in vivo assays affirmed the whole mechanism of miR-612 in NF1. We indicated that miR-612 was significantly low in tumor tissues and cells. Mechanism experiments confirmed that miR-612 promotion repressed cell proliferation and migration, and induced cell apoptosis. Besides, NFKB1-regulated miR-612 targeted FAIM2. Spearman's correlation analysis validated the correlation between each two genes. Finally, rescue and in vivo assays affirmed that miR-612 targeted FAIM2 to regulate cellular activities of NF1. The current investigation uncovered the molecular mechanism underlying miR-612 in NF1, establishing miR-612 as a novel therapeutic target for the treatment of NF1 patients.
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