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

M. Liang, X.-C. Liu, T. Liu, W.-J. Li, J.-G. Xiang, D. Xiao, Y.-L. Zhang, M.-H. Zheng, C. Zhai, L. Chen, Y.-H. Bai

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

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• Oncology

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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