Evidence map›Paper›PMID 37716117›Full record

ReviewBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2023

Nuclear factor kappa B expression in non-small cell lung cancer.

Leilei Zhang, Claudia M Ludden, Alexander J Cullen, Kenneth D Tew, André Luís Branco de Barros, Danyelle M Townsend

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
9.1field-weighted citation impact, top 2% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 2 countries.

Leilei ZhangDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC, USA.
Claudia M LuddenDepartment of Drug Discovery and Experimental Sciences, Medical University of South Carolina, Charleston, SC, USA.
Alexander J CullenDepartment of Drug Discovery and Experimental Sciences, Medical University of South Carolina, Charleston, SC, USA.
Kenneth D TewDepartment of Cell and Molecular Pharmacology and Experimental Therapeutics, Medical University of South Carolina, Charleston, SC, USA.
André Luís Branco de BarrosDepartment of Clinical and Toxicological Analyses, Faculty of Pharmacy, Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais, Brazil.
Danyelle M TownsendDepartment of Drug Discovery and Experimental Sciences, Medical University of South Carolina, Charleston, SC, USA. Electronic address: townsed@musc.edu.
Medical University of South Carolina · USUniversidade Federal de Minas Gerais · BR

Funding

SOUTH CAROLINA COBRE IN OXIDANTS, REDOX BALANCE AND STRESS SIGNALINGP20GM103542 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI TEW, KENNETH D. · 2012 to 2020
$20.2M
NIGMS NIH HHS P20 GM103542
6 · The paper itself

Abstract

In this mini-review, we discuss the role of NF-κB, a proinflammatory transcription factor, in the expression of genes involved in inflammation, proliferation, and apoptosis pathways, and link it with prognosis of various human cancers, particularly non-small cell lung cancer (NSCLC). We and others have shown that NF-κB activity can be impacted by post-translational S-glutathionylation through reversible formation of a mixed disulfide bond between its cysteine residues and glutathione (GSH). Clinical data analysis showed that high expression of NF-κB correlated with shorter overall survival (OS) in NSCLC patients, suggesting a tumor promotion function for NF-κB. Moreover, NF-κB expression was associated with tumor stage, lymph node metastasis, and 5-year OS in these patients. NF-κB was over-expressed in the cytoplasm of tumor tissue compared to adjacent normal tissues. S-glutathionylation of NF-κB caused negative regulation by interfering with DNA binding activities of NF-κB subunits. In response to oxidants, S-glutathionylation of NF-κB also correlated with enhanced lung inflammation. Thus, S-glutathionylation is an important contributor to NF-κB regulation and clinical results highlight the importance of NF-κB in NSCLC, where NF-κB levels are associated with unfavorable prognosis.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsGene Expression RegulationHumansNF-kappa BProtein Processing, Post-TranslationalNF-kappa BGlutathionylationLung cancerNFkBP50P65Redox regulation

Identifiers

PMID37716117
PMCPMC10591792
OpenAlexW4386763248

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.