ReviewBiomedicines2018
Subunit-Specific Role of NF-κB in Cancer.
Review in Biomedicines, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
68 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- Efficacy ofFrontiers in pharmacology · 2024Pooled it
- IL-24 Induces Cell Dormancy and Oxaliplatin Resistance in Colon Cancer Cells by Activating NF-κB Pathway.Molecular carcinogenesis · 2026Article
- Phytochemical and Phytopharmacological Insights intoCurrent drug research reviews · 2026Review
- Pluripotent Cells Expressing APOE4 Exhibit a Pronounced Pro-Apoptotic Phenotype Accompanied by Markers of Hyperinflammation and a Blunted NF-κB Response.International journal of molecular sciences · 2025Article
- NSAID-encapsulated nanoparticles as a targeted therapeutic platform for modulating chronic inflammation and inhibiting cancer progression: a review.Inflammopharmacology · 2025Review
- Biological potential and mechanisms of Tea's bioactive compounds: An Updated review.Journal of advanced research · 2024Review
- NF-κB in Alzheimer's Disease: Friend or Foe? Opposite Functions in Neurons and Glial Cells.International journal of molecular sciences · 2024Review
- High-throughput sequencing analysis of differential microRNA expression in the process of blocking the progression of chronic atrophic gastritis to gastric cancer by Xianglian Huazhuo formula.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Transient interactions modulate the affinity of NF-κB transcription factors for DNA.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Serum Induces the Subunit-Specific Activation of NF-κB in Proliferating Human Cardiac Stem Cells.International journal of molecular sciences · 2024Article
- Downstream STING pathways IRF3 and NF-κB differentially regulate CCL22 in response to cytosolic dsDNA.Cancer gene therapy · 2024Article
- Nimbolide: promising agent for prevention and treatment of chronic diseases (recent update).Food & nutrition research · 2024Article
- Cancer-Preventive Activity ofCancers · 2023Article
- Natural Bacterial and Fungal Peptides as a Promising Treatment to Defeat Lung Cancer Cells.Molecules (Basel, Switzerland) · 2023Review
- EPO regulates neuronal differentiation of adult human neural-crest derived stem cells in a sex-specific manner.BMC neuroscience · 2023Article
- KSHV hijacks FoxO1 to promote cell proliferation and cellular transformation by antagonizing oxidative stress.Journal of medical virology · 2023Article
- The ideal treatment timing for diabetic retinopathy: the molecular pathological mechanisms underlying early-stage diabetic retinopathy are a matter of concern.Frontiers in endocrinology · 2023Review
- The application and research progress of anti-angiogenesis therapy in tumor immunotherapy.Frontiers in immunology · 2023Review
- NF-κB mediated regulation of tumor cell proliferation in hypoxic microenvironment.Frontiers in pharmacology · 2023Review
- Influence of Long Non-Coding RNA in the Regulation of Cancer Stem Cell Signaling Pathways.Cells · 2022Review
8 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
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription factor NF-κB is a key player in inflammation, cancer development, and progression. NF-κB stimulates cell proliferation, prevents apoptosis, and could promote tumor angiogenesis as well as metastasis. Extending the commonly accepted role of NF-κB in cancer formation and progression, different NF-κB subunits have been shown to be active and of particular importance in distinct types of cancer. Here, we summarize overexpression data of the NF-κB subunits RELA, RELB, and c-REL (referring to the v-REL, which is the oncogene of Reticuloendotheliosis virus strain T) as well as of their upstream kinase inhibitor, namely inhibitor of κB kinases (IKK), in different human cancers, assessed by database mining. These data argue against a universal mechanism of cancer-mediated activation of NF-κB, and suggest a much more elaborated mode of NF-κB regulation, indicating a tumor type-specific upregulation of the NF-κB subunits. We further discuss recent findings showing the diverse roles of NF-κB signaling in cancer development and metastasis in a subunit-specific manner, emphasizing their specific transcriptional activity and the role of autoregulation. While non-canonical NF-κB RELB signaling is described to be mostly present in hematological cancers, solid cancers reveal constitutive canonical NF-κB RELA or c-REL activity. Providing a linkage to cancer therapy, we discuss the recently described pivotal role of NF-κB c-REL in regulating cancer-targeting immune responses. In addition, current strategies and ongoing clinical trials are summarized, which utilize genome editing or drugs to inhibit the NF-κB subunits for cancer treatment.
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What OpenQuestion holds
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.