Research Paper Advance Articles

CCNA2 and KIF23 are molecular targets for the prognosis of adenoid cystic carcinoma

Yongbin Di1, *, , Haolei Zhang2, *, , Bohao Zhang2, , Tianke Li3, *, , Dan Li2, *, ,

  • 1 Department of Stomatology, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei 050030, P.R. China
  • 2 Department of Otolaryngology, Head and Neck Surgery, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei 050030, P.R. China
  • 3 Department of Stomatology, The Fourth Hospital of Hebei Medical University, Shijiazhuang, Hebei 050011, P.R. China
* Equal contribution

Received: June 2, 2023       Accepted: December 12, 2023       Published: April 2, 2024
How to Cite

Copyright: © 2024 Di et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Objective: Adenoid cystic carcinoma (ACC) is a tumor type derived from glands. However, relationship between CCNA2 and KIF23, and adenoid cystic carcinoma remains unclear.

Methods: GSE36820 and GSE88804 profiles for ACC were obtained from the Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were identified, and Weighted Gene Co-expression Network Analysis (WGCNA) was conducted. Subsequently, the construction and analysis of protein–protein interaction (PPI) network, functional enrichment analysis, and Gene Set Enrichment Analysis (GSEA) were performed. A gene expression heat map was generated to visually depict the expression difference of core genes between adenoid cystic carcinoma and normal samples. TargetScan was employed to identify miRNAs that regulated central DEGs. Western blotting (WB) was conducted for cell verification.

Results: A total of 885 DEGs were identified. GO and KEGG analyses revealed their main enrichment in responses to chemical stimuli, cell proliferation, tissue development, and regulation of cell proliferation. The GO and KEGG results indicated significant enrichment in aldosterone-regulated sodium reabsorption, the cell cycle, and the PPAR signaling pathway. Notably, core genes (CCNA2 and KIF23) were found to be highly expressed in Adenoid Cystic Carcinoma samples and expressed at low levels in normal samples. WB validated the overexpression of CCNA2 and KIF23 in the Adenoid Cystic Carcinoma group, confirming the protein-level changes associated with cell cycle, metastasis, apoptosis, and inflammatory factors in Adenoid Cystic Carcinoma groups with gene overexpression and knockout.

Conclusions: CCNA2 and KIF23 exhibit high expression levels in ACC, suggesting their potential role as molecular targets for this malignancy.


ACC: adenoid cystic carcinoma; GEO: gene expression omnibus; DEGs: differentially expressed genes; WGCNA: weighted gene co-expression network analysis; PPI: protein–protein interaction; GSEA: Gene Set Enrichment Analysis; GO: gene ontology; KEGG: Kyoto Encyclopedia of Genes and Genomes; MAD: Median Absolute Deviation; STRING: Search Tool for the Retrieval of Interacting Genes; EMT: epithelial-mesenchymal transformation; CDK2: cyclin-dependent kinase 2; KIF23: Kinesin family member 23; MCC: Maximum Clique Centrality; MNC: Maximum Network Connectivity; ACC: adenoid cystic carcinoma group; ACC_OE: adenoid cystic oncogene overexpression group; ACC_KO: adenoid cystic oncogene knockout group.