ArticleJCI insight2024
Critical and distinct roles of cell type-specific NF-κB2 in lung cancer.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 8 citations in OpenAlex.
- NF-κB inducing kinase (NIK) deletion accelerates KRAS-driven pancreatic cancer in association with tumor microenvironment remodeling.Cell death & disease · 2026Article
- An Advanced Single-Cell RNA Sequencing (scRNA-seq) Protocol Utilizing Custom-Designed Multiplexing.Bio-protocol · 2026Article
- Enhanced HIF-1α cooperation by a human RORγt mutant potentiates Th17 pathogenicity.Cell reports · 2026Article
- PDLIM2 repression: a common mechanism in viral lung infection.ImmunoHorizons · 2026Article
- PDLIM2 in Lung Adenocarcinoma Metastasis.bioRxiv : the preprint server for biology · 2025Article
- PDLIM2 Repression: A Common Mechanism in Viral Lung Infection.bioRxiv : the preprint server for biology · 2025Article
- NanoPDLIM2-Based Combination Therapy for Lung Cancer Treatment in Mouse Preclinical Studies.Bio-protocol · 2025Article
- Myeloid PDLIM2 repression as a common mechanism of infection susceptibility in lung diseases.Frontiers in immunology · 2025Article
- NF-κB RelA is a cell-intrinsic metabolic checkpoint restricting glycolysis.Cell & bioscience · 2024Article
- NF-κB1 deficiency promotes macrophage-derived adrenal tumors but decreases neurofibromas in HTLV-I LTR-Tax transgenic mice.PloS one · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Different from the well-studied canonical NF-κB member RelA, the role of the noncanonical NF-κB member NF-κB2 in solid tumors, and lung cancer in particular, is poorly understood. Here we report that in contrast to the tumor-promoting role of RelA, NF-κB2 intrinsic to lung epithelial and tumor cells had no marked effect on lung tumorigenesis and progression. On the other hand, NF-κB2 limited dendritic cell number and activation in the lung but protected lung macrophages and drove them to promote lung cancer through controlling activation of noncanonical and canonical NF-κB, respectively. NF-κB2 was also required for B cell maintenance and T cell activation. The antitumor activity of lymphocyte NF-κB2 was dominated by the protumor function of myeloid NF-κB2; thus, NF-κB2 has an overall tumor-promoting activity. These studies reveal a cell type-dependent role for NF-κB2 in lung cancer and help understand the complexity of NF-κB action and lung cancer pathogenesis for better design of NF-κB-targeted therapy against this deadliest cancer.
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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.