CDCA2 promotes tumorigenesis and induces radioresistance in oesophageal squamous cell carcinoma cells

Mol Med Rep. 2021 Jul;24(1):530. doi: 10.3892/mmr.2021.12169. Epub 2021 May 26.

Abstract

Cell division cycle‑associated 2 (CDCA2) overexpression has been demonstrated to serve a significant role in tumorigenesis in certain types of cancer. Nevertheless, its role in tumour proliferation and radioresistance in oesophageal squamous cell carcinoma (ESCC) remains to be elucidated. Thus, the present study aimed to elucidate these roles. Data were downloaded from The Cancer Genome Atlas (TCGA) to compare the gene expression profiles. The expression of CDCA2 was higher in ESCC tissues compared with normal tissues. Gene set enrichment analysis was performed based on the ESCC cohorts in TCGA database. This demonstrated that higher expression of CDCA2 was significantly associated with the expression of related components of the cell cycle phase transition and G2/M phase transition pathways. Collectively, the results revealed that CDCA2 could serve as an underlying target to regulate tumour growth and radioresistance among patients with ESCC.

Keywords: DNA repair; The Cancer Genome Atlas; cell cycle phase; gene set enrichment analysis; radiosensitivity; tumorigenesis.

MeSH terms

  • Animals
  • Carcinogenesis / genetics*
  • Carrier Proteins / antagonists & inhibitors
  • Carrier Proteins / genetics*
  • Cell Cycle / genetics
  • Cell Cycle Proteins / antagonists & inhibitors
  • Cell Cycle Proteins / genetics*
  • Cell Line, Tumor
  • Cell Proliferation / genetics
  • Esophageal Neoplasms / genetics*
  • Esophageal Squamous Cell Carcinoma / genetics*
  • Gene Expression Regulation, Neoplastic / genetics
  • Gene Knockdown Techniques
  • Humans
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Nuclear Proteins / antagonists & inhibitors
  • Nuclear Proteins / genetics*
  • Radiation Tolerance / genetics*
  • Up-Regulation
  • Xenograft Model Antitumor Assays

Substances

  • CDCA2 protein, human
  • Carrier Proteins
  • Cell Cycle Proteins
  • Nuclear Proteins

Grants and funding

The present study was supported by the National Natural Science Foundation of China [grant no. 81672983 (BA16)].