Downregulation of CDCA5 Can Inhibit Cell Proliferation, Migration, and Invasion, and Induce Apoptosis of Prostate Cancer Cells

Crit Rev Eukaryot Gene Expr. 2021;31(1):29-40. doi: 10.1615/CritRevEukaryotGeneExpr.2020036803.

Abstract

Background: Prostate cancer (PC) is the most common form of cancer in males and accounts for many cancer-related deaths. Human cell division cycle associated 5 (CDCA5) may be a useful marker for predicting tumor metastasis and therapeutic target for the treatment of PC patients. In this study, we investigated the role of CDCA5 in prostate cancer progression. Immunohistochemistry was performed on 20 prostate cancer tissue samples.

Method: We performed immunohistochemistry on 20 prostate cancer tissue samples. CDCA5, a gene that is differentially expressed in prostate cancer, was screened with The Cancer Genome Atlas database. In both DU145 and PC-3 cells, CDCA5 levels consistently affected cell proliferation, colony formation, apoptosis, migration, and invasion.

Result: CDCA5 knockdown significantly inhibited PC cell proliferation, migration, and invasion. Furthermore, the apoptosis of DU145 and PC-3 cells was significantly increased after CDCA5 downregulation. Further investigations revealed that CDCA5 may participate in the development of PC through interaction with TWIST1, CDH1, and CDH2.

Conclusion: The present results provide a novel insight into the important and multifaceted role of CDCA5 in PC, indicating that CDCA5 is a promising biomarker and therapeutic target for PC.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / genetics*
  • Adaptor Proteins, Signal Transducing / metabolism*
  • Animals
  • Apoptosis
  • Biomarkers, Tumor
  • Carcinoma / genetics
  • Carcinoma / metabolism
  • Carcinoma / pathology
  • Cell Cycle
  • Cell Cycle Proteins / genetics*
  • Cell Cycle Proteins / metabolism*
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Down-Regulation
  • Gene Expression Regulation, Neoplastic*
  • Gene Knockdown Techniques / methods
  • Humans
  • Immunohistochemistry
  • Male
  • Mice
  • Mice, Nude
  • Prognosis
  • Prostatic Neoplasms / genetics*
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / pathology
  • Reactive Oxygen Species / metabolism

Substances

  • Adaptor Proteins, Signal Transducing
  • Biomarkers, Tumor
  • CDCA5 protein, human
  • Cell Cycle Proteins
  • Reactive Oxygen Species