ArticleFrontiers in oncology2022
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Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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
10 citing papers in PubMed, 12 citations in OpenAlex.
- Zinc finger protein-associated gene signature serves as a potential predictor for prognosis and therapeutic response in lung adenocarcinoma.Amino acids · 2026Article
- The role of m6A modification in non-small cell lung cancer: functional insights and impact on therapy resistance.Cancer cell international · 2025Review
- IGF2BP1 promotes the progression of head and neck squamous cell carcinoma by activating PI3K/AKT/mTOR signaling pathway and inducing epithelial-mesenchymal transition.World journal of surgical oncology · 2025Article
- Epitranscriptomics Regulation of CD70, CD80, and TIGIT in Cancer Immunity.International journal of molecular sciences · 2025Article
- m6A-Mediated Stabilization of PRMT9 mRNA by IGF2BP1 Drives Proliferation and Metastasis in Lung Adenocarcinoma.Analytical cellular pathology (Amsterdam) · 2025Article
- Prognostic Significance of R-Loops in Lung Adenocarcinoma: Implications for Immune Response and Drug Sensitivity.Cancer management and research · 2025Article
- A novel nomogram model for lung adenocarcinoma subtypes based on RNA-modification regulatory genes.Heliyon · 2024Article
- A novel subtype based on driver methylation-transcription in lung adenocarcinoma.Journal of cancer research and clinical oncology · 2024Article
- Implications of GCLC in prognosis and immunity of lung adenocarcinoma and multi-omics regulation mechanisms.BMC pulmonary medicine · 2024Article
- Implications of different cell death patterns for prognosis and immunity in lung adenocarcinoma.NPJ precision oncology · 2023Article
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 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Lung adenocarcinoma (LUAD), the most common type of lung cancer, poses a significant threat to the life of patients. N6-methyladenosine modification is the most abundant epigenetic modification and may play an important role in the lung carcinogenesis. IGF2BP1 is a newly discovered m6A-binding protein, but little is known about its role in LUAD. Methods: Data from TCGA, GEO, Kaplan-Meier Plotter, and GEPIA databases were systematically analyzed to access the expression and prognostic value of IGF2BP1 on LUAD. Real-time polymerase chain reaction, Western blot, and immunohistochemistry were performed to detect the mRNA and protein level of IGF2BP1 in LUAD tissues and para-carcinoma tissues. Functional cell experiments, including Cell Counting Kit-8 assay, Transwell invasion assay, wound healing assay, Annexin V-FITC/PI double-staining assay, and TUNEL assay, were used to investigate the functions of IGF2BP1 on LUAD cell proliferation, invasion, migration, and apoptosis, respectively. The top 50 genes that were positively or negatively related to the expression of IGF2BP1 were identified, and pathway enrichment analysis was performed. m Result: 16 m Conclusions: Our findings demonstrate that IGF2BP1 plays a contributory role in the development and progression of LUAD. IGF2BP1 has the potential to become a prognostic predictor and therapeutic target for LUAD.
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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.