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GLI-1 facilitates the EMT induced by TGF-β1 in gastric cancer

M Liang¹, X-C Liu, T Liu

¹Department of Oncology Surgery, 3201 Hospital, affiliated to College of Medicine, Xi'an Jiaotong University, Hanzhong City, China. byh819@163.com.

European Review for Medical and Pharmacological Sciences

|November 8, 2018

Abstract

Objective:

To explore how GLI-1 affects the EMT induced by TGF-β1 in gastric cancer.

Materials And Methods:

Following 24 hours of culture of SGC-7901 cells in presence of TGF-β1, we observed the changes in morphology as well as mRNA and protein expressions of GLI-1, E-cadherin and Vimentin by RT-PCR and Western blot. Transwell assay was conducted to evaluate the changes in invasion ability of SGC-7901 cells. Then, SGC-7901 cells were co-treated with TGF-β1 and GANT 61, and changes of the above indexes were also detected using the corresponding methods.

Results:

In presence of TGF-β1, EMT was initiated in SGC-7901 cells EMT with increased cell invasion ability, and the mRNA and protein expressions of E-cadherin were downregulated, while those of the GLI-1 and Vimentin were upregulated. Conversely, the co-treatment of TGF-β1 and GANT 61 suppressed the increased cell invasion ability induced only by TGF-β1, and the changes in mRNA and protein expressions of these factors were abolished.

Conclusions:

We found that GLI-1 facilitates the EMT induced by TGF-β1 in SGC-7901 cells, which may serve as a potential target in developing the clinical treatment of gastric cancer.

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