Background: Hepatocellular carcinoma (HCC) is the most frequent kind of liver cancer with high morbidity and mortality rates worldwide. Altered expression of BUB1 (budding uninhibited by benzimidazole 1) gene leads to chromosome instability and aneuploidy. This study investigated the expression of BUB1 and its prognostic value as well as its correlation with immune cell infiltration and immune checkpoints in HCC.
Results: Using the Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) databases, we found that BUB1 was up-regulated in HCC, thus prompting us to validate this observation by immunohistochemistry on 57 HCC paraffin embedded tissues from Wuxi No.2 People's Hospital. Kaplan-Meier survival analysis revealed that HCC patients with high BUB1 expression had shorter overall survival (OS) time as well as progression-free interval (PFI), and disease-specific survival (DSS) time compared to the patients with low BUB1 expression. Besides, STRING database showed that the top 10 co-expression genes were mainly involved in the regulation of cell division during the mitosis. Gene Ontology (GO) analysis and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that BUB1 had a connection to cancer related pathways. Lastly, The Tumor Immune Estimation Resource (TIMER) analysis found that BUB1 was positively related to immune cell infiltration and some immune checkpoint gene in HCC.
Clinical Trial Number: Not applicable.
Conclusions: Our present study demonstrated that BUB1 is a potential prognostic biomarker, and BUB1 may play a role in the tumor immune microenvironment in HCC.
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http://dx.doi.org/10.1186/s12865-025-00698-4 | DOI Listing |
BMC Immunol
March 2025
Department of Gastroenterology, Jiangnan University Medical Center, Wuxi No.2 People's Hospital, Wuxi, Jiangsu Province, China.
Background: Hepatocellular carcinoma (HCC) is the most frequent kind of liver cancer with high morbidity and mortality rates worldwide. Altered expression of BUB1 (budding uninhibited by benzimidazole 1) gene leads to chromosome instability and aneuploidy. This study investigated the expression of BUB1 and its prognostic value as well as its correlation with immune cell infiltration and immune checkpoints in HCC.
View Article and Find Full Text PDFMol Biol Res Commun
January 2025
Department of Genetics, Reproductive Biomedicine Research Center, Royan Institute for Reproductive Biomedicine, ACECR, Tehran, Iran.
Chromosome aberrations certainly aneuploidie are the cause of the majority of spontaneous abortions in humans. (budding uninhibited by benzimidazole 1) and (BUB1 mitotic checkpoint serine/threonine kinase B) are two key proteins mediating spindle-checkpoint activation that play a role in the inhibition of the anaphase-promoting complex/ cyclosome (APC/C), delaying the onset of anaphase and ensuring proper chromosome segregation. This study aimed to evaluate the probable roles of and pathogenic variants in abortion of the fetuses with aneuploidy.
View Article and Find Full Text PDFbioRxiv
February 2025
Cell and Developmental Biology Center, National Heart, Lung, and Blood Institute, National Institutes of Health; Bethesda, Maryland 20894, USA.
Hybrid incompatibility can lead to lethality and sterility of F1 hybrids, contributing to speciation. Here we found that female hybrids between and mice are sterile due to the failure of homologous chromosome separation in oocyte meiosis I, producing aneuploid eggs. This non-separation phenotype was driven by the mis-localization of the cohesin protector, SGO2, along the chromosome arms instead of its typical centromeric enrichment, resulting in cohesin over-protection.
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
February 2025
Department of Gastroenterology Surgery, Yichang Central People's Hospital, The First College of Clinical Medical Science, China Three Gorges University, 443000 Yichang, Hubei, China.
Background: Dysregulated metabolic pathways, including glycolysis and a compromised DNA damage response (DDR), are linked to the progression of colorectal cancer (CRC). The mitotic arrest deficient-like 2 () and aurora kinase B () genes play roles in cell cycle regulation and the DDR, making them potential targets for CRC therapy.
Methods: Differential expression analysis was performed using The Cancer Genome Atlas-Colon Adenocarcinoma (TCGA-COAD) and GSE47074 datasets.
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