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Updated: May 10, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
10:37

Induction and Analysis of Epithelial to Mesenchymal Transition

Published on: August 27, 2013

Selenate induces epithelial-mesenchymal transition in a colorectal carcinoma cell line by AKT activation

Takanori Tsukamoto1, Susumu Hama1, Kentaro Kogure1

  • 1Department of Biophysical Chemistry, Kyoto Pharmaceutical University, Misasagi Nakauchi-cho 5, Yamashina-ku, Kyoto 607-8414, Japan.

Experimental Cell Research
|June 18, 2013
PubMed

Insights

Sodium selenate shows anticancer effects in colorectal cancer cells but can also induce epithelial-mesenchymal transition (EMT). This EMT, linked to AKT activation, may counteract therapeutic benefits, requiring careful consideration for drug development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Selenite exhibits potent anticancer properties.
  • Sodium selenate has shown modest therapeutic effects in prostate cancer.
  • Selenate activates protein phosphatase 2A, inhibiting pathways like PI3K/AKT.

Purpose of the Study:

  • To investigate the anticancer effects of sodium selenate in DLD-1 colorectal carcinoma cells.
  • To explore the impact of sodium selenate on cell viability, apoptosis, and signaling pathways.
  • To assess the potential for sodium selenate to induce epithelial-mesenchymal transition (EMT).

Main Methods:

  • Cell viability and apoptosis assays were performed.
  • DLD-1 cells were treated with varying concentrations of sodium selenate and selenite.
  • Expression of EMT markers (TWIST1, vimentin, E-cadherin) and AKT activation were analyzed.
  • An AKT inhibitor (Akti-1/2) was used to assess the role of AKT in selenate-induced effects.

Main Results:

  • Sodium selenate decreased cell viability and increased apoptosis in DLD-1 cells (IC50 = 0.88mM), but was less potent than selenite (IC50 = 0.0061mM).
  • At lower concentrations (0.04-0.16mM), selenate induced EMT, characterized by altered cell morphology and motility.
  • Selenate-induced EMT involved AKT activation, increased TWIST1 and vimentin expression, and decreased E-cadherin.
  • AKT inhibition suppressed selenate-induced EMT-associated cell motility and invasion.

Conclusions:

  • Sodium selenate demonstrates anticancer potential in colorectal cancer cells.
  • However, selenate can induce EMT, potentially mediated by AKT activation, which may have deleterious effects.
  • The induction of EMT by sodium selenate warrants careful consideration for its therapeutic application.
Keywords:
50% inhibitory concentrationAKTAKT inhibitorAkti-1/2EMTEpithelial–mesenchymal transitionIC(50)PI3KPIP3PP2APTENProtein phosphatase 2ASodium selenateTWIST1Vimentinepithelial-mesenchymal transitionphosphatase and tensin homologphosphatidylinositol 3-kinasephosphatidylinositol-3,4,5-trisphosphateprotein phosphatase 2AqRT-PCRquantitative reverse-transcription polymerase chain reaction

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