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Upregulation of Twist is involved in Gli1 induced migration and invasion of hepatocarcinoma cells

  • Juan Li EMAIL logo , Yuting He , Yuan Cao EMAIL logo , Yan Yu , Xiaolong Chen , Xiaojuan Gao and Qiuyue Hu
Published/Copyright: June 19, 2018

Abstract

Hedgehog (Hh) signaling is involved in the progression of hepatocellular carcinoma (HCC), while its detailed mechanisms are not well illustrated. Our present study revealed that the expression of Gli1, while not Gli2 or Gli3, is significantly increased in HCC cell lines and 20/28 (71.4%) HCC tissues as compared with their corresponding controls. Over expression of Gli1 can promote the migration, invasion and epithelial-mesenchymal transition (EMT) of HCC cells. Gli1 can increase the expression of Twist, while not other EMT transcription factors such as Snail, ZEB1 or Slug. Gli1 increases the transcription of Twist while it has no significant effect on the protein or mRNA stability. Chromatin immunoprecipitation-polymerase chain reaction confirms that Gli1 can directly bind to the promoter of Twist, in which the third binding site is essential for Gli1 induced transcription. Collectively, our data suggest that upregulation of Twist is involved in Gli1 induced migration and invasion of HCC cells.

Keywords: EMT; Gli1; HCC; migration; Twist

aJuan Li and Yuting He: These authors contributed equally to this work.
Corresponding authors: Dr. Juan Li, Department of Infectious Diseases, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China

Award Identifier / Grant number: 81702927

Funding statement: The National Natural Science Foundation of China (Funder Id: 10.13039/501100001809, 81702927); the Medical Science and Technology research project of Henan province (201702001); Key Scientific Research Project of Henan Higher Education Institutions of China (18A320038); Joint research fund of the First Affiliated Hospital of Zhengzhou University and the Dalian institute of Chemical Physics, Chinese Academy of Science.

  1. Conflict of interest statement: The authors declare no conflict of interest.

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Received: 2018-01-23
Accepted: 2018-04-11
Published Online: 2018-06-19
Published in Print: 2018-07-26

©2018 Walter de Gruyter GmbH, Berlin/Boston

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