ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
RBM15-mediated m6A modification of XPR1 promotes the malignant progression of lung adenocarcinoma.
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 9 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.
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Who cites it
9 citing papers in PubMed.
- Isoquercitrin suppresses neuronal ferroptosis in ischemic stroke via SIRT1-mediated deacetylation of H3K9 at the RBM15 promoter.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Article
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- A Novel YTHDF2/SIGMAR1 Axis in Astrocytes Regulates Neuroinflammation and Cognitive Impairment in Diabetic Encephalopathy.Inflammation · 2026Article
- Article
- Prognostic potential of N6-methyladenosine methylation-associated genes in lung adenocarcinoma.Translational cancer research · 2025Article
- Article
- RBM15 promotes hypoxia/reoxygenation-induced ferroptosis in human cardiomyocytes by mediating m6A modification of ACSL4.Hereditas · 2025Article
- RBM15-mediated mFrontiers in cell and developmental biology · 2025Review
- Summary of the mechanism of ferroptosis regulated by m6A modification in cancer progression.Frontiers in cell and developmental biology · 2025Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) is a leading cause of cancer-related deaths worldwide. The poor prognosis of LUAD is attributed to its aggressive biological behavior and resistance to conventional therapies. Xenotropic and polytropic retrovirus receptor 1 (XPR1), a member of the XPR family, has been implicated in the pathogenesis of various malignancies, including LUAD. However, the regulatory mechanism of XPR1 in LUAD remains elusive. The study employed immunohistochemistry (IHC) and western blotting to analyze the protein expression of XPR1, RNA binding motif protein 15 (RBM15) and nuclear proliferation marker (ki-67) in LUAD tissues and cells. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression of XPR1, glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11), and RBM15. Cell proliferation was assessed using a CCK-8 assay, colony-formation assay, and 5-Ethynyl-2'-deoxyuridine assay. Cell invasion and apoptosis were evaluated through transwell assay and flow cytometry, respectively. Caspase 3 activity and Fe
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Identifiers
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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.