ArticleCommunications biology2024
NIPBL-mediated RAD21 facilitates tumorigenicity by the PI3K pathway in non-small-cell lung cancer.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.
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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.
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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
5 citing papers in PubMed, 4 citations in OpenAlex.
- Epigenetics in lung cancer precision medicine: from bench to bedside-a narrative review.Translational lung cancer research · 2026Review
- Bioinformatic analysis and experimental validation of the function of mitogen-activated protein kinase in esophageal cancer.Discover oncology · 2026Article
- Aberrant cohesin function in Saccharomyces cerevisiae activates Mcd1 degradation to promote cell lethality.PLoS genetics · 2025Article
- Aberrant cohesin function inbioRxiv : the preprint server for biology · 2025Article
- A Cornelia de Lange syndrome NIPBL 5'-UTR mutation reduces cell proliferation in anBiomedical reports · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
Abstract
It is urgent to identify novel early diagnostic markers and therapeutic targets for non-small-cell lung cancer (NSCLC), which accounts for 85% of lung cancer cases and has a 5-year survival rate of 4-17%. Here, chromatin immunoprecipitation (ChIP) was used to identify DNA‒protein interactions, RNA methylation was determined by methylated RNA immunoprecipitation (MeRIP), RNA stability was tested by an RNA decay assay. We showed that RAD21, a member of the cohesin complex, is upregulated in NSCLC tissues and cell lines and found to be an independent prognostic factor for overall survival (OS) of NSCLC patients. Mechanistically, the cohesin loading factor Nipped-B-Like Protein (NIPBL) promoted RAD21 gene transcription by enhancing histone H3 lysine 27 (H3K27) demethylation via recruiting lysine demethylase 6B (KDM6B) to the RAD21 gene promoter. RAD21 enhanced phosphatidylinositol 3-kinase (PI3K) gene transcription, and NIPBL reversed the effect of enhancer of zeste 2; catalytic subunit of polycomb repressive complex 2 (EZH2) on RAD21-mediated PI3K gene transcription by disrupting the association between EZH2 and RAD21. Moreover, NIPBL level was increased by stabilization of its transcripts through mRNA methylation. These findings highlight the oncogenic role of RAD21 in NSCLC and suggest its use as a potential diagnostic marker and therapeutic target for NSCLC.
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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.