ArticleAmerican journal of cancer research2023
CENPH overexpression promotes the progression, cisplatin resistance, and poor prognosis of lung adenocarcinoma via the AKT and ERK/P38 pathways.
Article in American journal of cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 8 citations in OpenAlex.
- Shared genetic regulators and diagnostic biomarkers in gallbladder stone and cholangiocarcinoma: A comprehensive comparative transcriptomic analysis.Translational oncology · 2026Article
- Classifying Molecular Subtypes and Establishing a Prognosis Model using Oxidative Stress-related Genes for Lung Adenocarcinoma.Current medicinal chemistry · 2026Article
- Centromere Protein F in Tumor Biology: Cancer's Achilles Heel.Cancer medicine · 2025Review
- ZDHHC5 as a central regulator in a palmitoylation-associated prognostic model for lung adenocarcinoma: insights from pan-cancer and experimental analyses.Frontiers in immunology · 2025Article
- CENP-H as a new prognostic biomarker for tumors: a real-world literature review.Frontiers in oncology · 2025Review
- Downregulation of PAQR3 expression predicts poor prognosis of patients with pan-cancer: a meta-analysis.Frontiers in oncology · 2025Review
- Comprehensive bioinformatics analysis of prognosis and immunotherapy in lung adenocarcinoma.Journal of thoracic disease · 2024Article
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10 authors at 4 institutions in 1 country.
Funding
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Abstract
Overexpression of centromere protein H (CENPH) promotes cancer growth and progression. However, the roles and underlying mechanisms have not been elucidated. Therefore, we aim to explore the roles and mechanisms of CENPH in lung adenocarcinoma (LUAD) progression by using comprehensive data analysis and cell experiments. In this study, the relationship between CENPH expression, which was obtained from the TCGA, and GTEx databases, and the prognosis and clinical characteristics of LUAD patients was analyzed, and the diagnostic values of CENPH was evaluated. CENPH-related risk models and nomograms were constructed to evaluate the prognosis of LUAD via Cox and LASSO regression analysis. The roles and mechanisms of CENPH in LUAD cells were studied using CCK-8 assay, wound healing and migration tests, and western blotting. The relationship between CENPH expression and immune microenvironment and RNA modifications was explored through correlation analysis. We found that CENPH was overexpressed in LUAD tissues, and tumors with diameter >3 cm, lymph node metastasis, distant metastasis, late stage, men, and dead cancer patients. Increased expression of CENPH was related to the diagnosis, poor survival rate, disease specific survival rate, and progression of LUAD. CENPH-related nomograms and risk models could predict the survival rate of LUAD patients. Inhibiting the expression of CENPH in LUAD cells decreased their migration, proliferation, and invasion, and promoted their sensitivity to cisplatin, which was related to the downregulation of p-AKT, p-ERK, and p-P38. However, there was no effect on AKT, ERK, and P38. Enhanced expression of CENPH was significantly correlated with immune score, immune cells, cell markers, and RNA modifications. In conclusion, CENPH was strongly expressed in LUAD tissues and was associated with poor prognosis, immune microenvironment, and RNA modifications. CENPH overexpression could enhance cell growth and metastasis and promote resistance to cisplatin via the AKT and ERK/P38 pathways, indicating its potential as a biomarker for the prognosis of LUAD.
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Identifiers
37293159PMC10244101W4379966764What OpenQuestion holds
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