ArticleJournal of molecular histology2025
Identification of the oncogenic role of centromere protein M in non-small cell lung cancer via CDC20/MYBL2/Wnt signaling pathways.
Article in Journal of molecular histology, 2025. 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
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Who cites it
2 citing papers in PubMed.
- MYBL2 promotes malignant phenotypes and M2-like macrophage polarization through CCL2 in non-small cell lung cancer.Molecular and cellular biochemistry · 2026Article
- Targeting centromere protein M represses cell growth and mobility via inactivating AKT pathway but less affects BRAF inhibitor sensitivity in cutaneous melanoma.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer remains the most prevalent carcinoma with a high mortality rate, yet the underlying mechanisms driving pulmonary neoplasia and disease progression are not fully understood. In our study, we conducted a comprehensive analysis of the transcriptome profiles and clinicopathological characteristics of 515 patients diagnosed with non-small cell lung cancer (NSCLC) from the TCGA database. We identified a significant upregulation of centromere protein M (CENPM) in NSCLC tissues, which was positively correlated with poor prognosis. Furthermore, overexpression of CENPM markedly promoted cell proliferation and increased the tumorigenic potential of NSCLC cell lines (A549/NCI-H1299), leading to accelerated tumor progression and reduced survival time in tumor-bearing mice. Mechanistically, CENPM activated the Wnt/β-catenin signaling pathway via the cell division cycle 20 (CDC20)/MYB proto-oncogene-like 2 (MYBL2) axis. Inhibition of either Wnt signaling or the CDC20/MYBL2 axis attenuated the tumorigenic potential and proliferative effects induced by CENPM. Our findings underscore the critical role of CENPM in driving NSCLC development and suggest that CENPM could serve as a novel biomarker for predicting NSCLC progression in clinical settings.
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