ArticleTranslational cancer research2022
The prognostic value and mechanisms of centromere protein M in patients with lung adenocarcinoma.
Article in Translational cancer research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- A dual-mechanism model of Selinexor in DLBCL: p53 reactivation and metabolic reprogramming.Journal of translational medicine · 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
- Expression, Prognostic Value, and Biological Function of CENPM in Colon Adenocarcinoma.Current medicinal chemistry · 2026Article
- Identification of the oncogenic role of centromere protein M in non-small cell lung cancer via CDC20/MYBL2/Wnt signaling pathways.Journal of molecular histology · 2025Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Centromere protein M (CENPM) has been reported to exert important roles in promoting tumor initiation and progression. However, the expression, effect, impact on prognosis and underlying mechanism of CENPM in lung adenocarcinoma (LUAD) remain unclear. Methods: Seventy-eight paired clinical samples of LUAD and corresponding adjacent non-tumor (ANT) tissues were obtained. The clinical pathological data and clinical outcome were tested, including univariate and multivariate Cox regression model. The relationship between CENPM expression and LUAD prognosis were identified according to the data obtained from the Cancer Genome Atlas (TCGA) database. Then, we explored the protein and mRNA levels of Results: CENPM was significantly upregulated in LUAD patients compared with healthy controls, and CENPM upregulation was relevant to the higher pathological stages and poor survival rates in our LUAD patients. The bioinformatics analysis also revealed similar trends. CENPM could promote cell proliferation, cause alterations in cell cycle progression, enhance cell migration and invasion capacity, promote apoptosis in LUAD cell lines and promote the growth of xenografts in nude mice via regulation of AKT1/mTOR signaling pathway. Conclusions: CENPM was upregulated in LUAD patients, and it correlated with higher pathological stages and poor survival rates. CENPM could affect cell proliferation, cell cycle, cell migration and invasion capacity, and apoptosis in LUAD cell lines via regulation of AKT1/mTOR signaling pathway.
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