ArticleFEBS open bio2023
Minichromosome maintenance proteins in lung adenocarcinoma: Clinical significance and therapeutic targets.
Article in FEBS open bio, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Circulating microRNAs as Biomarkers of Brain Metastases in Lung Cancer: A Pilot Study.Journal of clinical medicine · 2026Article
- miR-378a-5p targets FGR to suppress proliferation, invasion and migration in lung adenocarcinoma cells.Translational cancer research · 2025Article
- Transcription factor E2F1 promotes non-small cell lung cancer progression by activating the PI3K/AKT pathway through MCM4.Journal of cardiothoracic surgery · 2025Article
- [miR-2110 Affects the Biological Behaviors of Lung Adenocarcinoma by Regulating CDT1].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Article
- Starting DNA Synthesis: Initiation Processes during the Replication of Chromosomal DNA in Humans.Genes · 2024Review
- Identification of Tumor-SuppressiveCancers · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is the most common cause of cancer-related death worldwide, accounting for 1.8 million deaths annually. Analysis of The Cancer Genome Atlas data showed that all members of the minichromosome maintenance (MCM) family (hexamers involved in DNA replication: MCM2-MCM7) were upregulated in lung adenocarcinoma (LUAD) tissues. High expression of MCM4 (P = 0.0032), MCM5 (P = 0.0032), and MCM7 (P = 0.0110) significantly predicted 5-year survival rates in patients with LUAD. Simurosertib (TAK-931) significantly suppressed the proliferation of LUAD cells by inhibiting cell division cycle 7-mediated MCM2 phosphorylation. This finding suggested that MCM2 might be a therapeutic target for LUAD. Moreover, analysis of the epigenetic regulation of MCM2 showed that miR-139-3p, miR-378a-5p, and miR-2110 modulated MCM2 expression in LUAD cells. In patients with LUAD, understanding the role of these miRNAs may improve prognoses.
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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.