Clinical value and potential mechanisms of BUB1B up-regulation in nasopharyngeal carcinoma

• Main Authors: Li-Ting Qin (Author), Si-Wei Huang (Author), Zhi-Guang Huang (Author), Yi-Wu Dang (Author), Ye-Ying Fang (Author), Juan He (Author), Yi-Tong Niu (Author), Cai-Xing Lin (Author), Ji-Yun Wu (Author), Zhu-Xin Wei (Author)
• Format: Book
• Published: BMC, 2022-12-01T00:00:00Z.
• Subjects: article
• Online Access: Connect to this object online.
• Notes: 10.1186/s12920-022-01412-8; 1755-8794
• Keywords: Nasopharyngeal carcinoma (NPC); BUB1 mitotic checkpoint serine/threonine kinase B (BUB1B); Standard mean deviation (SMD); Immunohistochemical (IHC); Internal medicine; RC31-1245; Genetics; QH426-470
• Source: BMC Medical Genomics, Vol 15, Iss 1, Pp 1-15 (2022)

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.