CDK4/RB/E2Fs axis as potential therapeutic target of endometrial cancer

Biomed Pharmacother. 2020 May:125:109870. doi: 10.1016/j.biopha.2020.109870. Epub 2020 Feb 4.

Abstract

The increasing incidence rate and decreasing patients' five-year survival rate for endometrial cancer (EC) in recent decades highlight the necessity for further investigation of the molecular characteristics involved in cancer initiation and progression. In this study, we found that the pathways associated with mitotic cell cycle were enriched in primary EC samples versus normal endometrial samples through analyzing RNA-seq data of The Cancer Genome Atlas (TCGA). The messenger RNA (mRNA) expression of three activator E2Fs (E2F1, E2F2, and E2F3) and their target genes increased significantly in EC samples. Additionally, the high transcriptional activity of activator E2Fs was associated with poor survival, advanced clinical stage, high histologic grade, and aggressive histological type. We further demonstrated that E2Fs hyperactivation correlated with DNA hypomethylation and high cyclin-dependent kinase 4 (CDK4) expression. Moreover, abemaciclib, a selective CDK4 inhibitor, significantly inhibited the proliferation rates of human EC cell lines in vitro. And, abemaciclib also obviously inhibited EC cell growth in nude mice model. Collectively, our data suggest that the misregulation of CDK4/RB/E2Fs axis is associated with EC oncogenesis, and abemaciclib is a potential targeted drug for EC.

Keywords: CDK4; Cell cycle; E2F1; E2F2; E2F3; Endometrial cancer.

MeSH terms

  • Animals
  • Antineoplastic Agents / pharmacology
  • Antineoplastic Agents / therapeutic use
  • Biomarkers, Tumor*
  • Cell Cycle / genetics
  • Cell Line, Tumor
  • Cell Proliferation
  • Cell Transformation, Neoplastic / genetics
  • Cell Transformation, Neoplastic / metabolism
  • Cyclin-Dependent Kinase 4 / genetics
  • Cyclin-Dependent Kinase 4 / metabolism*
  • DNA Copy Number Variations
  • Disease Models, Animal
  • E2F Transcription Factors / genetics
  • E2F Transcription Factors / metabolism*
  • Endometrial Neoplasms / drug therapy
  • Endometrial Neoplasms / etiology*
  • Endometrial Neoplasms / metabolism*
  • Endometrial Neoplasms / pathology
  • Female
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Mice
  • Molecular Targeted Therapy
  • Mutation
  • Prognosis
  • Protein Binding
  • Retinoblastoma Protein / genetics
  • Retinoblastoma Protein / metabolism*
  • Signal Transduction / drug effects
  • Transcriptional Activation
  • Xenograft Model Antitumor Assays

Substances

  • Antineoplastic Agents
  • Biomarkers, Tumor
  • E2F Transcription Factors
  • Retinoblastoma Protein
  • CDK4 protein, human
  • Cyclin-Dependent Kinase 4