ArticleOncology reports2018
DNA damage induced by human CD40 ligand mutant promotes senescence and induces demethylation of GATA4 in lung cancer.
Article in Oncology reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Cellular senescence in lung cancer immune microenvironment and senotherapeutic opportunities.iScience · 2026Review
- Comprehensive Analysis of Expression and Prognostic Value of GATAs in Lung Cancer.Journal of Cancer · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ligand of CD40, known as CD154 or CD40L, is the key to immunostimulatory and anticancer activity, but how CD40L affects cellular senescence is unclear. Thus, we studied a membrane‑stable mutant form CD40L (CD40L‑M) to explore tumor growth and cellular senescence in CD40‑positive NSCLC cells. We found that CD40L‑M‑expressing cells had senescent characteristics, including reduced cell proliferation and enlargement, increased SA‑β‑gal staining activity, and overexpression of several cell cycle regulators p53 and p21. In addition, expression of GATA4 was restored, and the NF‑κB signaling pathway was activated in the CD40L‑M‑induced senescent cells. Mechanistic analyses revealed that CD40L‑M expression triggered the ATM/Chk2 DNA damage response, which mediated cell senescence and GATA4 activation. Knockdown of GATA4 reversed CD40L‑M‑induced senescence and decreased NF‑κB activity. Thus, CD40L‑M contributes to induction of cell senescence in CD40‑positive NSCLC cells, and GATA4 is a switch to activate the NF‑κB pathway, which is positively regulated by DNA damage response (DDR) signaling kinases. Collectively, CD40L‑M‑induced senescence may be a barrier to the growth of lung cancer cells.
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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.