ArticleCancer reports (Hoboken, N.J.)2023
High expression of centromere protein N as novel biomarkers for gastric adenocarcinoma.
Article in Cancer reports (Hoboken, N.J.), 2023. 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, 9 citations in OpenAlex.
- Diagnostics and immunological function of CENPN in human tumors: from pan-cancer analysis to validation in breast cancer.Translational cancer research · 2025Article
- Knockdown of CENPM activates cGAS-STING pathway to inhibit ovarian cancer by promoting pyroptosis.BMC cancer · 2024Article
- CENPN contributes to pancreatic carcinoma progression through the MDM2-mediated p53 signaling pathway.Archives of medical science : AMS · 2024Article
- High expression of centromere protein N as novel biomarkers for gastric adenocarcinoma.Cancer reports (Hoboken, N.J.) · 2023Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe role and mechanism of centromeric protein N (CENP-N), which has been associated with the development of various cancer types, are yet unclear in stomach adenocarcinoma (STAD).
methodsData from the Cancer Genome Atlas and Genotype-Tissue Expression were used to determine whether CENP-N expression was altered in STAD tumors compared to normal tissues. Xiantao was used to perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG) enrichment analysis on CENP-N. The relationship between CENP-N expression and immune cell infiltration was assessed using TCGA database. The expression of CENP-N in STAD and surrounding tissues was confirmed using immunohistochemical staining and the correlation between CENP-N expression and clinicopathological characteristics was examined. The effects of CENP-N knockdown by siRNA on proliferation were measured by CCK-8 and EdU assays in AGS cells. Following siRNA transfection, flow cytometry was performed to evaluate cell cycle and apoptotic alterations in AGS cells. The effect of CENP-N knockdown on the expression level of related proteins was detected by Westren blot.
resultsCENP-N was highly expressed in STAD tissues, which was confirmed by our immunohistochemistry results. The degree of invasion, TNM stage, and lymph node metastases were all strongly associated with CENP-N expression. CENP-N was essential for the cell cycle, DNA replication, chromosomal segregation, and nuclear division; there was a positive correlation between CENP-N expression and infiltrating Th2 and NK CD56dim cells and a negative correlation between CENP-N expression and mast, pDC, NK, and B cell infiltration. When CENP-N expression in AGS cells was knocked down, cell proliferation dramatically reduced (p < .05) and the percentage of cells in the S and G2-M phases decreased significantly (p < .05). Silencing CENP-N significantly promoted the apoptosis of AGS cells (p < .05). Mechanistic investigations showed that silencing CENP-N expression may inhibit STAD proliferation through the Cyclin E1 and promote STAD apoptosis through the Bcl-2/Bax.
conclusionAccording to our data, CENP-N acts as an oncogene in STAD and may be a viable therapeutic target.
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