Curcumin Inhibits Proliferation and Epithelial-Mesenchymal Transition in Lens Epithelial Cells through Multiple Pathways

Biomed Res Int. 2020 Mar 31:2020:6061894. doi: 10.1155/2020/6061894. eCollection 2020.

Abstract

Background: Posterior capsule opacification (PCO), a complication of extracapsular lens extraction surgery that causes visual impairment, is characterized by aberrant proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Curcumin, exerting inhibitive effects on cell proliferation and EMT in cancer, serves as a possible antidote towards PCO.

Methods: Cellular proliferation of LECs after treatment of curcumin was measured with MTT assay and flow cytometry. The transcriptional and expressional levels of proteins related to proliferation and EMT of LECs were quantified by western blotting and real-time PCR.

Results: Curcumin was found to suppress the proliferation of LECs by inducing G2/M arrest via possible inhibition of cell cycle-related proteins including CDK1, cyclin B1, and CDC25C. It had also inactivated proliferation pathways involving ERK1/2 and Akt pathways in LECs. On the other hand, curcumin downregulated the EMT of LECs through blocking the TGF-β/Smad pathway and interfering Notch pathway which play important roles in PCO.

Conclusions: This study shows that curcumin could suppress the proliferation and EMT in LECs, and it might be a potential therapeutic protection against visual loss induced by PCO.

MeSH terms

  • Apoptosis / drug effects
  • Blotting, Western
  • CDC2 Protein Kinase / antagonists & inhibitors
  • CDC2 Protein Kinase / genetics
  • CDC2 Protein Kinase / metabolism
  • Cell Cycle / drug effects
  • Cell Division
  • Cell Proliferation / drug effects*
  • Curcumin / pharmacology*
  • Cyclin B1 / antagonists & inhibitors
  • Cyclin B1 / genetics
  • Cyclin B1 / metabolism
  • Dose-Response Relationship, Drug
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Epithelial-Mesenchymal Transition / drug effects*
  • G2 Phase
  • Gene Expression Regulation
  • Humans
  • Lens, Crystalline / drug effects
  • Proto-Oncogene Proteins c-akt / antagonists & inhibitors
  • Proto-Oncogene Proteins c-akt / genetics
  • Proto-Oncogene Proteins c-akt / metabolism
  • Signal Transduction / drug effects
  • Transforming Growth Factor beta2 / antagonists & inhibitors
  • Transforming Growth Factor beta2 / metabolism

Substances

  • Cyclin B1
  • Transforming Growth Factor beta2
  • Proto-Oncogene Proteins c-akt
  • CDC2 Protein Kinase
  • CDK1 protein, human
  • Curcumin