Oncotarget

Research Papers:

PTTG1 cooperated with GLI1 leads to epithelial-mesenchymal transition in esophageal squamous cell cancer

Wang Feng, Xuan Xiaoyan, Li Shenglei, Liu Hongtao and Jiang Guozhong _

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Oncotarget. 2017; 8:92388-92400. https://doi.org/10.18632/oncotarget.21343

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Abstract

Wang Feng1, Xuan Xiaoyan2, Li Shenglei3, Liu Hongtao4 and Jiang Guozhong3

1Department of Oncology, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China

2Department of Immunology, School of Basic Medical Science, Zhengzhou University, Zhengzhou 450001, P.R. China

3Department of Pathology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, P.R. China

4Laboratory for Cell Biology, School of Life Sciences of Zhengzhou University, Zhengzhou 450001, P.R. China

Correspondence to:

Jiang Guozhong, email: guozhongjiang@zzu.edu.cn

Keywords: esophageal squamous cell cancer, pituitary tumor-transforming gene-1, glioma-associated oncogene homolog1, epithelial-mesenchymal transition

Received: May 02, 2017     Accepted: July 18, 2017     Published: September 27, 2017

ABSTRACT

Pituitary tumor-transforming gene-1 (PTTG1) could acquire its metastasis-promoting effects via inducing epithelial-mesenchymal transition (EMT). However, its role and mechanism in EMT in esophageal squamous cell cancer (ESCC) had not been clearly elucidated. Here, we demonstrated that PTTG1 was overexpressed in ESCC cell lines and tissues especially those with lymph node metastasis. Down regulation of PTTG1 levels dampened the ESCC cells invasion, migration, proliferation ability and colony formation in vitro and inhibited the growth of mouse xenograft model of ESCC cells in vivo. In addition, our in vitro and in vivo experiments consistently showed that decreased PTTG1 led to the inhibition of EMT process. Glioma-associated oncogene homolog1 (GLI1), a key factor in HH-GLI signaling pathway, was also overexpressed in ESCC cells and tissues. Mechanistic studies demonstrated that decreased PTTG1 mitigated the expression levels of GLI1 in vitro and in vivo and ChIP assay also indicated that PTTG1 cooperated with GLI1 by binding to its promoter. Furthermore, overexpression of GLI1 rescued the EMT inhibited by down regulation of PTTG1 in vitro. Together, these data suggested that PTTG1 promoted the invasion ability of ESCC cells via EMT, more important, PTTG1 participated in EMT via activating the expression of GLI1 in ESCC. PTTG1 could be a candidate biomarker for defining ESCC metastasis and useful target for therapy.


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