ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
ETS1 promotes cisplatin resistance of NSCLC cells by promoting GRP78 transcription.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- ETS1-EGR2 facilitates renal cell carcinoma progression by activating NOTCH signalling.Clinical and translational medicine · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Non-small cell lung cancer (NSCLC) is a common malignant tumor characterized by rapid growth and invasive power. Glucose regulatory protein 78 (GRP78) is important in cancer cell progression. Here, this study aimed to explore the effect and mechanism of GRP78 on cisplatin (DDP) resistance of NSCLC cells. qRT-PCR and Western blot detected the expression of genes and proteins. Flow cytometry was used to analyze endoplasmic reticulum stress (ERS) induced by DDP in NSCLC. Cell proliferation and apoptosis were examined using cell counting kit-8 (CCK8), cell cloning, and flow cytometry, respectively. Chromatin immunoprecipitation assay (CHIP) and dual-luciferase reporter assays were performed to determine the binding of ETS1 and GRP78 promoter. Mouse xenograft models were constructed for in vivo analysis. ERS was induced by DDP in NSCLC cells. GRP78 were upregulated in DDP-resistant NSCLC tissues, and knockdown of GRP78 suppressed DDP resistance, clone formation, promoted apoptosis, and inhibited ERS in DDP-resistant NSCLC cells. ETS1 knockdown repressed GRP78 expression and NSCLC tumor growth. Interestingly, ETS1 played a role in DDP-resistant NSCLC via GRP78. ETS1 inhibits cisplatin sensitivity of NSCLC cells by promoting GRP78 transcription.
Indexed as
Identifiers
39521757What 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.