PancreasGli1 promotes transforming growth factor-beta1– and epidermal growth factor–induced epithelial to mesenchymal transition in pancreatic cancer cells
Section snippets
Tissue samples
This study was approved by the institutional review board of the First Hospital of China Medical University, and every participant signed a consent form. Sixty-two formalin-fixed and paraffin-embedded pancreatic ductal adenocarcinoma tissues were obtained from patients at the First Hospital of China Medical University between 2006 and 2011. All diagnoses were confirmed pathologically, and all tissue samples were analyzed according to the 7th edition of the Union for International Cancer Control
The clinicopathologic significance of and relationships between Gli1, MMP9, E-cad, and Vimentin in PC tissues
In 62 PC tissue samples, the expressions of Gli1 in the nucleus and cytoplasm, MMP9 and Vimentin in the cytoplasm, and E-cad in the membrane were considered for scoring (E-cad–negative expression and localization in the cytoplasm were considered as abnormal expression) (Fig 1). IHC showed that the positive expression rates of Gli1, MMP9, E-cadherin (membrane location), and Vimentin in the PC tissue samples were 53.2% (33/62), 58.1% (36/62), 38.7% (24/62), and 29.0% (18/62), respectively.
Discussion
EMT has been shown to contribute to PC tumor formation and metastasis, but the mechanisms by which EMT is regulated are not completely clear.2, 16 Aberrant activation of the Hedgehog (Hh)-Gli1 axis has been described as a key mediator of cancer metastasis via EMT.17, 18, 19 Our previous study showed that Gli1 promoted cell invasion and migration of PC.7 Thus, we hypothesize that Hh-Gli1 regulates PC invasion and motility in an EMT-dependent manner.
However, the roles of Gli1 in EMT regulation in
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Qingfeng Liu and Weiwei Sheng contributed equally to this work.
The authors declare no conflicts of interest.
This work was supported by the Social Development Program from Shenyang Science and Technology Bureau, China (no. F15-139-9-19) and by the Chinese National Science Foundation for Youth Scholar (no. 81401941 to Weiwei Sheng).