ArticleCancer cell2013
The pivotal role of IKKα in the development of spontaneous lung squamous cell carcinomas.
Article in Cancer cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 112 citations in OpenAlex.
- Opposed expression of IKKα: loss in keratinizing carcinomas and gain in non-keratinizing carcinomas.Oncotarget · 2015Pooled it
- A Non-Canonical Role of SMAD4 in Regulating 3D Genome Architecture to Inhibit Lung Squamous Cell Carcinoma Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The IKKα-regulated microRNA miR-9-5p mediates lung cancer growth and invasiveness via CDH1/Wnt/β-catenin signalling.Cell death discovery · 2026Article
- The roles of IKKα in normal physiology and cancer.Cell communication and signaling : CCS · 2026Review
- Isoleucine and valine regulate the BCAA antagonism by influencing insulin function in broiler chickens.Journal of animal science and biotechnology · 2026Article
- The Role of A20 in Cancer: Friend or Foe?Cells · 2025Review
- Mutations disrupting the kinase domain of IKKα lead to immunodeficiency and immune dysregulation in humans.The Journal of experimental medicine · 2025Article
- Defective kinase activity of IKKα leads to combined immunodeficiency and disruption of immune tolerance in humans.Nature communications · 2024Article
- TET2-STAT3-CXCL5 nexus promotes neutrophil lipid transfer to fuel lung adeno-to-squamous transition.The Journal of experimental medicine · 2024Article
- Nuclear factor kappa B expression in non-small cell lung cancer.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2023Review
- p63: a crucial player in epithelial stemness regulation.Oncogene · 2023Review
- TNFR1 and TNFR2, Which Link NF-κB Activation, Drive Lung Cancer Progression, Cell Dedifferentiation, and Metastasis.Cancers · 2023Review
- The role of macrophages in non-small cell lung cancer and advancements in 3D co-cultures.eLife · 2023Article
- Pre-clinical lung squamous cell carcinoma mouse models to identify novel biomarkers and therapeutic interventions.Frontiers in oncology · 2023Review
- A TNFR1-UBCH10 axis drives lung squamous cell carcinoma dedifferentiation and metastasis through a cell-autonomous signaling loop.Cell death & disease · 2022Article
- IKKα-deficient lung adenocarcinomas generate an immunosuppressive microenvironment by overproducing Treg-inducing cytokines.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Histologic transformation in lung cancer: when one door shuts, another opens.Therapeutic advances in medical oncology · 2022Review
- Preclinical Models for the Study of Lung Cancer Pathogenesis and Therapy Development.Cold Spring Harbor perspectives in medicine · 2021Review
- Mapping lung squamous cell carcinoma pathogenesis through in vitro and in vivo models.Communications biology · 2021Review
- NLRP3 Inhibition Ameliorates Severe Cutaneous Autoimmune Manifestations in a Mouse Model of Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy-Like Disease.The Journal of investigative dermatology · 2021Article
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
21 authors at 4 institutions in 1 country.
Funding
Abstract
Here, we report that kinase-dead IKKα knockin mice develop spontaneous lung squamous cell carcinomas (SCCs) associated with IKKα downregulation and marked pulmonary inflammation. IKKα reduction upregulated the expression of p63, Trim29, and keratin 5 (K5), which serve as diagnostic markers for human lung SCCs. IKKα(low)K5(+)p63(hi) cell expansion and SCC formation were accompanied by inflammation-associated deregulation of oncogenes, tumor suppressors, and stem cell regulators. Reintroducing transgenic K5.IKKα, depleting macrophages, and reconstituting irradiated mutant animals with wild-type bone marrow (BM) prevented SCC development, suggesting that BM-derived IKKα mutant macrophages promote the transition of IKKα(low)K5(+)p63(hi) cells to tumor cells. This mouse model resembles human lung SCCs, sheds light on the mechanisms underlying lung malignancy development, and identifies targets for therapy of lung SCCs.
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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.