NUSAP1 promotes pancreatic ductal adenocarcinoma progression by drives the epithelial-mesenchymal transition and reduces AMPK phosphorylation

• Published in: BMC cancer Vol. 24; no. 1; pp. 87 - 16
• Main Authors: Liu, Yuan, Tang, Rong, Meng, Qing-Cai, Shi, Si, Xu, Jin, Yu, Xian-Jun, Zhang, Bo, Wang, Wei
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 16.01.2024; BioMed Central; BMC
• Subjects: Adenocarcinoma; Analysis; B cells; Beta cells; Bioinformatics; Biotechnology; Care and treatment; CD8 antigen; Cell cycle; Cell division; Cell migration; Cell proliferation; Chromosomes; Datasets; Development and progression; Differentially expressed genes; DNA microarrays; Functional enrichment analysis; Gene expression; Genes; Genetic aspects; Genomes; Genomics; Health aspects; Heterozygosity; Homologous recombination; Loss of heterozygosity; Lymphocytes T; Medical prognosis; Molecular modelling; Mutation; Nucleoli; Pancreas; Pancreatic cancer; Pancreatic ductal adenocarcinoma; Pathogenesis; Phosphorylation; Prognosis; Protein expression; Protein-protein interactions; Proteins; Protein‒protein interaction; Scientific equipment and supplies industry; Software; Stem cells; Survival analysis; T cells; Transcriptomes; Tumorigenesis; China; United States; Survival analysis; Differentially expressed genes; Functional enrichment analysis; Pancreatic ductal adenocarcinoma; Protein‒protein interaction
• ISSN: 1471-2407; 1471-2407
• DOI: 10.1186/s12885-024-11842-5

Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, and its molecular mechanisms are unclear. Nucleolar and spindle-associated protein 1 (NUSAP1), an indispensable mitotic regulator, has been reported to be involved in the development of several types of tumors. The biological function and molecular mechanism of NUSAP1 in PDAC remain controversial. This study explored the effects and mechanism of NUSAP1 in PDAC. Differentially expressed genes (DEGs) were screened. A protein‒protein interaction (PPI) network was constructed to identify hub genes. Experimental studies and tissue microarray (TMA) analysis were performed to investigate the effects of NUSAP1 in PDAC and explore its mechanism. Network analysis revealed that NUSAP1 is an essential hub gene in the PDAC transcriptome. Genome heterogeneity analysis revealed that NUSAP1 is related to tumor mutation burden (TMB), loss of heterozygosity (LOH) and homologous recombination deficiency (HRD) in PDAC. NUSAP1 is correlated with the levels of infiltrating immune cells, such as B cells and CD8 T cells. High NUSAP1 expression was found in PDAC tissues and was associated with a poor patient prognosis. NUSAP1 promoted cancer cell proliferation, migration and invasion, drives the epithelial-mesenchymal transition and reduces AMPK phosphorylation. NUSAP1 is an essential hub gene that promotes PDAC progression and leads to a dismal prognosis by drives the epithelial-mesenchymal transition and reduces AMPK phosphorylation.