ArticleBMC medical genomics2022
Clinical value and potential mechanisms of BUB1B up-regulation in nasopharyngeal carcinoma.
Article in BMC medical genomics, 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, 4 citations in OpenAlex.
- Potential of non-specific blood biomarkers combined with EBV-specific antibodies for triaging in nasopharyngeal carcinoma screening.Scientific reports · 2026Article
- Integrative Bioinformatics Analysis for Targeting Hub Genes in Hepatocellular Carcinoma Treatment.Current genomics · 2025Article
- Revealing the Potential of Solamargine for Anti Metastasis and Angiogenesis Inhibition in Nasopharyngeal Carcinoma.Journal of inflammation research · 2025Article
- Comprehensively analyzing the genetic alterations, and identifying key genes in ovarian cancer.Oncology research · 2023Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Nasopharyngeal carcinoma (NPC) has insidious onset, late clinical diagnosis and high recurrence rate, which leads to poor quality of patient life. Therefore, it is necessary to further explore the pathogenesis and therapy targets of NPC. BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B) was found to be up-regulated in a variety of cancers, but only two previous study showed that BUB1B was overexpressed in NPC and the sample size was small. The clinical role of BUB1B expression and its underlying mechanism in NPC require more in-depth research. Immunohistochemical samples and public RNA-seq data indicated that BUB1B protein and mRNA expression levels were up-regulated in NPC, and summary receiver operating characteristic curve indicated that BUB1B expression level had a strong ability to distinguish NPC tissues from non-NPC tissues. Gene ontology and Kyoto Encyclopedia of genes and genomes were performed and revealed that BUB1B and its related genes were mainly involved in cell cycle and DNA replication. Protein- Protein Interaction were built to interpret the BUB1B molecular mechanism. Histone deacetylase 2 (HDAC2) could be the upstream regulation factor of BUB1B, which was verified by Chromatin Immunoprecipitation Sequencing samples. In summary, BUB1B was highly expressed in NPC, and HDAC2 may affect cell cycle by regulating BUB1B to promote cancer progression.
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Registered trials
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