High expression of centromere protein N as
novel biomarkers for gastric adenocarcinoma
Xiaojie Wang1,2, Keyuan Zhang1,2,
Cun Fu 1,2, Fei Wu1, Junjie
Zhang1, Bin Han3, Hai
Pan4, Lan Luan1*
1 Department of Pathology, Central Hospital Affiliated
to Shenyang Medical College, Shenyang, China.
2 Basic Medical School, Shenyang Medical College,
Shenyang, China.
3 Department of Urology, Shengjing Hospital of China
Medical University, Shenyang, China.
4 Central Laboratory, Central Hospital Affiliated to
Shenyang Medical College, Shenyang, China.
* Correspondence: Lan Luan
luanlan33@symc.edu.cn
Keywords: CENPN; gastric adenocarcinoma; proliferation; cycle;
apoptosis.
Abstract
Background: The role and mechanism of centromeric protein N
(CENPN), which has been associated with the development of various
cancer types, are yet unclear in Gastric adenocarcinoma (STAD).
Methods: Data from The Cancer Genome Atlas and Genotype Tissue
Expression were used to examine the expression of CENPN in STAD and
neighboring tissues. Xiantao Academic was used to perform Gene
Ontology(GO) and Kyoto Encyclopedia of Genes and Genomes(KEGG)
enrichment analysis on CENPN. By reviewing TCGA database, the
relationship between CENPN expression and immune cell infiltration was
assessed. The expression of CENPN in STAD and surrounding tissues was
confirmed by immunohistochemical staining, and the correlation between
CENPN expression and clinicopathological characteristics was examined.
CENPN was depleted in AGS cells with siRNAs, and its impact on
proliferation was measured by CCK-8 and EdU assays. Following siRNA
transfection, flow cytometry was performed to identify cell cycle and
apoptotic alterations in AGS cells.
Results: CENPN was highly expressed in STAD tissues. The degree
of invasion, TNM stage, and lymph node metastases were all substantially
linked with CENPN expression. GO|KEGG Enrichment analysis
revealed that CENPN was essential for the cell cycle, DNA replication,
chromosomal segregation, and nuclear division, among other important
signaling pathways. Further investigation revealed a positive
correlation between CENPN expression and Th2 cells and NK CD56dim cells
and a negative correlation between CENPN expression and mast cells , pDC
cells,NK cells and B cells. When CENPN expression in AGS cells was
knocked down, cell proliferation dramatically reduced, and the
percentage of cells in the S and G2-M phases decreased significantly. In
addition, compared to the control group, the proportion of apoptotic AGS
cells significantly increased after downregulating the expression level
of CENPN.
Conclusion: According to our data, CENPN acts as an oncogene in
STAD and may be a viable therapeutic target.