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09.12.2015 | Original Article | Ausgabe 5/2016

Tumor Biology 5/2016

Upregulation of PTEN suppresses invasion in Tca8113 tongue cancer cells through repression of epithelial–mesenchymal transition (EMT)

Tumor Biology > Ausgabe 5/2016
Siming Xie, Zhiyuan Lu, Yanzhu Lin, Lijia Shen, Cao Yin
Wichtige Hinweise
Siming Xie, Zhiyuan Lu and Yanzhu Lin contributed equally to this work.


We previously discovered that the expression of the tumor suppressor phosphatase and tensin homolog (PTEN) was downregulated in the majority patients with tongue squamous cell carcinoma (TSCC). The aim of this study was to investigate the role of PTEN overexpression in the regulation of epithelial–mesenchymal transition (EMT) of the tongue squamous carcinoma cell line Tca8113 as well as explore the underlying mechanism. GV230 (containing the PTEN gene) and empty vectors were transfected into Tca8113 cells. After stable transfection, the messenger RNA (mRNA) and protein levels of PTEN were validated using quantitative real-time PCR (qPCR) and Western blot analysis. The growth and cell cycle were analyzed using Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. The invasion ability was measured with a transwell assay. The effects of PTEN overexpression on EMT and Hedgehog signaling were assessed by comparing Tca8113-PTEN cells with control and negative control cell groups. We found that PTEN expression was significantly upregulated after transfection. Meanwhile, upregulated PTEN inhibited the proliferation and invasion of Tca8113 cells. In addition, we observed changes in the EMT- and Hedgehog-associated proteins. These data demonstrated that PTEN upregulation could reduce invasion by inhibiting the process of EMT in Tca8113 cells, which might be related to the Hedgehog signaling pathway.

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