Effects of PTEN gene silencing on invasion and EMT in oral squamous carcinoma Tca8113 cells

J Oral Pathol Med. 2017 Jan;46(1):31-38. doi: 10.1111/jop.12461. Epub 2016 Sep 3.

Abstract

Aim: To investigate the impact of silencing of the PTEN gene using siRNA on the invasion, proliferation, cell cycle, and epithelial-mesenchymal transition of the Tca8113 cell line.

Methods: The established Tca8113 cell model with siRNA interference to silence the PTEN gene was used. The transfection efficiency was examined by RT-qPCR and Western blot analysis. CCK-8 assay was utilized to analyze the proliferation of Tca8113 cells and cell invasion was evaluated using a transwell assay. The cell cycle distribution was analyzed by flow cytometry. The protein expression levels of the epithelial-mesenchymal transition (EMT) markers E-cadherin and Vimentin and the EMT-related proteins β-catenin and TGF-β1 were analyzed by Western blot.

Results: The expression level of PTEN was significantly reduced in the PTEN-siRNA group. The invasiveness and proliferation rate of Tca8113 cells in the PTEN-siRNA group were significantly greater than those of the control and negative control groups. The expression levels of E-cadherin and β-catenin were reduced, whereas the expression levels of vimentin and TGFβ-1 were elevated in the PTEN-siRNA group compared with those of control and negative groups. These results were significantly different.

Conclusion: The silencing of PTEN by siRNA increased the proliferation and promoted cell invasion of Tca8113 cells. PTEN gene silencing may accelerate the EMT in Tca8113 cells.

Keywords: EMT; PTEN; Tca8113 cells; invasion; small interference RNA.

MeSH terms

  • Antigens, CD
  • Cadherins / metabolism
  • Carcinoma, Squamous Cell / genetics
  • Carcinoma, Squamous Cell / metabolism
  • Carcinoma, Squamous Cell / pathology*
  • Cell Cycle
  • Cell Line, Tumor
  • Cell Proliferation
  • Epithelial-Mesenchymal Transition / physiology*
  • Gene Silencing*
  • Humans
  • Mouth Neoplasms / genetics
  • Mouth Neoplasms / metabolism
  • Mouth Neoplasms / pathology*
  • Neoplasm Invasiveness / genetics
  • PTEN Phosphohydrolase / genetics*
  • PTEN Phosphohydrolase / physiology
  • RNA, Small Interfering*
  • Transfection
  • Transforming Growth Factor beta1 / metabolism
  • beta Catenin / metabolism

Substances

  • Antigens, CD
  • CDH1 protein, human
  • Cadherins
  • RNA, Small Interfering
  • TGFB1 protein, human
  • Transforming Growth Factor beta1
  • beta Catenin
  • PTEN Phosphohydrolase
  • PTEN protein, human