ArticleOncogenesis2016
NIK regulates MT1-MMP activity and promotes glioma cell invasion independently of the canonical NF-κB pathway.
Article in Oncogenesis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- MMP14-Dependent Activation of TGF-β Signaling Enhances Malignancies via Promoting Necroptosis in Glioblastoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- EZH2 functional dichotomy in reactive oxygen species-stratified glioblastoma.Neuro-oncology · 2025Article
- Cyanine Dye Conjugation Enhances Crizotinib Localization to Intracranial Tumors, Attenuating NF-κB-Inducing Kinase Activity and Glioma Progression.Molecular pharmaceutics · 2023Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Transcriptional induction of NF-κB-inducing kinase by E2F4/5 facilitates collective invasion of GBM cells.Scientific reports · 2023Article
- NF-κB-Inducing Kinase Governs the Mitochondrial Respiratory Capacity, Differentiation, and Inflammatory Status of Innate Immune Cells.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Mitochondrial dynamics in neurological diseases: a narrative review.Annals of translational medicine · 2023Review
- Transcriptional Induction of NF-kB-Inducing Kinase by E2F4/5 Facilitates Collective Invasion of Glioma Cells.Research square · 2023Article
- Review
- Article
- Non-Canonical NF-κB Signaling Stratifies LGG into Subtypes with Distinct Molecular and Cellular Characteristic and Survival Expectancy.International journal of general medicine · 2022Article
- TBK1 Inhibitor Exerts Antiproliferative Effect on Glioblastoma Multiforme Cells.Oncology research · 2021Article
- RelB and Neuroinflammation.Cells · 2021Review
- NIK promotes metabolic adaptation of glioblastoma cells to bioenergetic stress.Cell death & disease · 2021Article
- A Kinase Assay for Measuring the Activity of the NIK-IKK1 Complex Induced via the Noncanonical NF-κB Pathway.Methods in molecular biology (Clifton, N.J.) · 2021Article
- Targeting NF-κB-Inducing Kinase (NIK) in Immunity, Inflammation, and Cancer.International journal of molecular sciences · 2020Review
- Growth pattern of experimental glioblastoma.Histology and histopathology · 2020Article
- Differential impact of classical and non-canonical NF-κB pathway-related gene expression on the survival of breast cancer patients.Journal of Cancer · 2019Article
- Inhibitory-κB Kinase (IKK) α and Nuclear Factor-κB (NFκB)-Inducing Kinase (NIK) as Anti-Cancer Drug Targets.Cells · 2018Review
- miR-188 Inhibits Glioma Cell Proliferation and Cell Cycle Progression Through Targeting β-Catenin.Oncology research · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
A growing body of evidence implicates the noncanonical NF-κB pathway as a key driver of glioma invasiveness and a major factor underlying poor patient prognoses. Here, we show that NF-κB-inducing kinase (NIK/MAP3K14), a critical upstream regulator of the noncanonical NF-κB pathway, is both necessary and sufficient for cell-intrinsic invasion, as well as invasion induced by the cytokine TWEAK, which is strongly associated with tumor pathogenicity. NIK promotes dramatic alterations in glioma cell morphology that are characterized by extensive membrane branching and elongated pseudopodial protrusions. Correspondingly, NIK increases the phosphorylation, enzymatic activity and pseudopodial localization of membrane type-1 matrix metalloproteinase (MT1-MMP/MMP14), which is associated with enhanced tumor cell invasion of three-dimensional collagen matrices. Moreover, NIK regulates MT1-MMP activity in cells lacking the canonical NF-κB p65 and cRel proteins. Finally, increased expression of NIK is associated with elevated MT1-MMP phosphorylation in orthotopic xenografts and co-expression of NIK and MT1-MMP in human tumors is associated with poor glioma patient survival. These data reveal a novel role of NIK to enhance pseudopodia formation, MT1-MMP enzymatic activity and tumor cell invasion independently of p65. Collectively, our findings underscore the therapeutic potential of approaches targeting NIK in highly invasive tumors.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.